HY topic thread : notes - bunnybunch

[ArchivalUser]

HEMATOLOGY & ONCOLOGY
((Ferrous sulfate orally (May turn the stool BLACK but Guaiac test -ve)))
((Anemia of chronic disease))
. Osteoarthritis doesn't cause anemia of chronic disease !
. Exclude anemia of chronic disease if there is NORMAL ESR !
(("IRON DEFECIENCY ANEMIA" - "ALPHA THALASSEMIA MINOR" - "BETA THALASSEMIA MINOR"))
. Hematocrit < 30 % - Hematocrit > 30 % - Hematocrit > 30 %
. RDW ++ - RDW normal - RDW normal
. RBC count -- - RBC count normal - RBC count normal to ++
. No target cells - TARGET cells on smear - TARGET cells on smear
. -- serum iron & ferritin - Nor. to ++ iron & ferritin - Nor. to ++ iron & ferritin
. ++ TIBC - Normal TIBC - Normal TIBC
. Responds to iron supplem. - No response to iron supplementation
. Normal Hb Electrophoresis - Normal Hb Electrophoresis - ++ Hb A2 on Hb Electrophor.
((N.B. MECHANISMS OF ANEMIA IN MICROCYTIC HYPOCHROMIC DISEASES))
. -- fe intake & ++ blood loss -> IRON DEFECIENCY ANEMIA.
. Defective utilization of storage iron -> ANEMIA OF CHRONIC DISEASES.
. -- globin production -> THALASSEMIA.
. -- Heme synthesis -> LEAD POISONING & SIDEROBLASTIC ANEMIA.
((N.B. (1)))
. Folate & cobalamine (B12) are involved in the conversion of homocysteine to methionine.
. -- Vit. B12 or folic acid -> ++ Homocysteine level.
((N.B. (2)))
. Folic acid & vit. B12 defeciency can be distinguished by measuring Methyl Malonic acid!
. Vit B12 (Not folic acid) is involved in the conversion of MMA to succinyl coA.
. -- Vitamin B12 -> ++ MMA.
. -- Folic acid -> NORMAL MMA.
((N.B. (3)))
. Laboratory tests ------------> Prinicious anemia -------------> Folic acid defeciency
. Serum B12 level -------------> (--) -------------> Normal.
. Serum folic acid level ------> (Normal) -------------> (--).
. Serum LDH level -------------> (++) -------------> Normal. !!!
. Achlorhydria ----------------> present -------------> Absent.
. Schilling test --------------> +ve -------------> -ve.
. Methyl malonyl acid MMA -----> ++ -------------> Absent.
. Neurological signs ----------> ++ -------------> Absent.
((N.B. (4)))
. Alcohol abuse is the most common cause of nutritional folate defeciency in USA.
((N.B. (5)))
. Anemia of chronic kidney disease is due to erythropoietin deficiency.
. One must be careful to ensure adequate iron stores prior to erthropoietin replacement,
. Bec. the erythropoietin induced surge in RBCs production may consume much iron,
. precipitating an iron defecient state.
((N.B. (6)))
. A case of microcytic hypochromic anemia with -- iron & ferritin,
. The most common cause of iron deficiency anemia is GIT blood loss.
. Dietary iron deficiency & malabsorption of iron are rare causes.
. Iron supplementation helps to restore iron reserves but u must detect the cause !
. So .. perform test for occult blood in the stool.
((N.B. (7)))
. The most common cause of folic acid deficiency is NUTRITIONAL.
. Either due to poor diet or Alcoholism.
. May be caused by some drugs either by impairing its absorption (PHENYTOIN),
. or antagonizing its physiologic effect (Methotrexate - Trimethoprim).
((N.B. (8))
. PERINICIOUS ANEMIA:
. Most common cause of vit. B12 deficiency.
. Auto-antibodies against the gastric intrinsic factor required for B12 absorption.
. More in Northern Europeans.
. Associated other auto-immune diseases e.g. Autoimmune thyroiditis & Vitiligo.
. Shiny tongue due to atrophic glossitis.
. Shuffling broad-based gait ataxia.
. Neurological abnormalities with loss of pain & vibration sense.
. Peripheral blood smear -> Macro-ovalocytes, megaloblasts & hyper-segmented neutrophils.
. Dx -> Detection of Anti-intrinsic factor Abs.
((N.B. (9)))
. Total body stores of Vit.B12 in humans are 2-5 mg with min. daily requirement 6-9 micg.
. Animal products (meat & dairy) are the only dietary sources of vit. B12.
. It would take 4-5 years of a pure vegan diet to cause dietary deficiency.
. In contrast, Folate stores are smaller, clinical deficiency occur within 4-5 months.
((N.B. (10)))
. SCHILLING TEST:
. Used to detect the cause of vit. B12 defeciency.
. Used to differentiate dietary defeciency from perinicious anemia & malabsorption.
. In dietary defeciency,
. Oral radiolabelled Vit B12 is absorbed in the gut & excr. by kidneys in NORMAL amounts.
. But In Malabsorption,
. Oral radio-labelled Vit B12 is excreted in sub-normal amounts.
((SICKLE CELL ANEMIA))
. Cause of Osteomyelitis in sickle cell anemia is SALMONELLA !
. Cause of BM suppression in sickle cell anemia is PARVO B19 !
((HEMOGLOBIN SICKLE CELL DISEASE))
. Isosthenuria due to RBCs sickling in the vasa rectae of the inner renal medulla.
. The pt have to wake to urinate 2 - 3 times per night despite restricting fluid intake.
. No ttt.
((N.B. PYRUVATE KINASE DEFECIENCY))
-> can lead to similar presentation as G6PDD .. BUT:
-> Hemolysis not precipitated by sulfa drugs !
-> No bite cells on peripheral smear !
((PAROXYSMAL NOCTURNAL HEMOGLOBINURIA (PNH)))
. PORTAL VEIN THROMBOSIS may be the key to answer PNH case !
. Hemolytic anemia + Venous thrombosis = PNH.
((MACROVASCULAR TRAUMATIC HEMOLYSIS))
. ++ reticulocytes - ++ LDH - -- Haptoglobin (‘intra-vascular hemolytic anemia’).
. Fragmented RBCs.
. Chronic hemolysis -> iron loss -> Microcytic anemia.
. Due to mechanical trauma from artificial valves or calcified aortic valves.
((HERIDITARY SPHEROCYTOSIS vs. AUTOIMMUNE HEMOLYTIC ANEMIA))
. Peripheral blood smears in both conditions -> Spherocytes without central pallor.
. Both cause extravascular hemolytic anemia.
. Heriditary spherocytosis -> Autosomal dominant heriditary condition.
. AIHA -> Acquired condition.
. Spherocytosis -> +ve family H/O & -ve Coomb's test.
. AIHA -> -ve family H/O & +ve Coomb's test.
((PATHO-PHYSIOLOGIC MECHANISMS of ANEMIA in variable diseases))***IMP***
. Impaired DNA & purine synthesis -> Vitamin B12 defeciency.
. RBC membrane instability -> Heriditary spherocytosis.
. Impaired Hb synthesis -> Iron defeciency anemia, sickle cell anemia & Thalassemia.
. Impaired glutathione synthesis -> G6PDD.
. Mechanical injury to RBCs -> Hemolysis with artificial heart valves.
((CARBOXYHEMOGLOBINEMIA = CARBON MONOXIDE (CO) POISONING))
. H/O of environmental risk (Pt working in an enclosed space -> underground parking lot).
. Present with headache, nausea & dizziness.
. Exposure to CO from automobile exhaust.
. CO binds Hb with an affinity app. 250 times that of oxygen.
. -- in blood carrying oxygen capacity.
. As a compensation -> the body ++ RBCs production (++ HCT).
((OBSTRUCTIVE SLEEP APNEA (OSA) -> ++ ERYTHROPOIETIN PRODUCTION))
. Recurrent transient obstruction of the upper airway due to pharyngeal collapse.
. Obese or over-weight pts have excessive snoring, day time sleeping & morning headaches.
. Transient episodes of hypoxia -> sensed by the kidneys -> ++ Erythropoietin production.
. Erythropoietin ++ RBCs -> Polycythemia.
. OSA doesn't cause carboxyhemoglobinemia ! xxxxxxxxxxxxxx
((CHRONIC LYMPHOCYTIC LEUKEMIA (CLL)))
. Dx -> Peripheral blood smear -> SMUDGE cells "Ruptured nuclei of lymphocytes".

((POLYCYATHEMIA VERA (Pvera)))
. ++ incidence of peptic ulcerations (++ Histamine release from basophils).
. ++ incidence of gouty arthritis ( ++ cell turnover).
. Dx -> CBC "MARKEDLY HIGH HEMATOCRITE & low MCV" !!!
. Dx -> ABG "Absence of hypoxia".
. Dx -> -- Erythropoietin (Most important).
. ++ WBCs & ++ Platelets.
. ++ B 12 & ++ LAP levels.
. Tx -> Hydroxyurea to -- cell count.
. Tx -> Give daily Aspirin to prevent Thrombosis.
. High risk of thrombosis -> Due to ++ platelet count.
. High risk of bleeding -> Due to impaired platelet function
((N.B. . HERIDITARY TELANGIECTASIA = OSLER - WEBER - RENDU $YNDROME))
. Diffuse telangiectasia + Recurrent epistaxis + Wide spread AV MALFORMATIONs.
. AV malformations in lung -> Blood shunt from Rt to Lt side of the heart.
. AV shunts -> Chronic hypoxemia -> Reactive polycythemia (++ HCT).
((PLASMA CELL DISORDERS))
. ALL are characterized by ++ serum protein with normal albumin (GAMMA GAP).
((MONO-CLONAL GAMMOPATHY OF UNKNOWN SIGNIFICANCE (MGUS))
. Asymptomatic ++ of IgG on SPEP. (due to ++ ptn in old age).
. Elderly pt > 70 ys.
. MGUS require METASTATIC SKELETAL BONE X-RAY to exclude lytic lesions sugesting MM !
. No ttt.

((MONO-CLONAL GAMMOPATHY OF UNKNOWN SIGNIFICANCE Vs MULTIPLE MYELOMA))
(MGUS) (MM)
. Absence of anemia. . Anemia.
. Hypercalcemia. . Hypercalcemia.
. Renal insuffeciency. . Renal insuffeciency.
. Lytic lesions in bones. !!!! . Lytic lesions in bones.
. Serum monoclonal protein < 3 g/dl. . Serum monoclonal protein > 3 g/dl.
. < 10 % plasma cells in the bone marrow. . > 10 % plasma cells in the bone marrow.
. ++ B 2 microglobulin.
((TUMOR LYSIS $YNDROME))
. Ass. with tumors with high cell turn-over.
. Ex: Poorly differentiated lymphoma "Burkitt's lymphoma" & Leukemias "ALL".
. HYPER {phosphatemia - kalemia - uricemia}.
. HYPO {Calcemia}.
. Both potassium & phosphate r intra-cellular ions, so cell break down -> their release.
. Released phosphate binds calcium leading to hypocalcemia.
. Degradation of cell proteins -> ++ uric acid levels.
. TL$ may lead to fatal arrhythmias, ARF & sudden death.
. Tx -> Allopurinol greatly reduces the possibility of acute urate nephropathy.
((ASYMPTOMATIC LOCALIZED LYMPHADENOPATHY))
. Several non-tender rubbery cervical Lymph nodes.
. Most commonly in upper respiratory tract infection.
. Commonly observed in children & young adults.
. Tx -> OBSERVATION !

((INFECTIOUS MONONUCLEOSIS (IM)))
. Acute, benign, self limiting lymphoproliferative condition.
. Caused by Epstein Barr virus (EBV).
. EBV is transmitted by close contact to infected oro-tracheal secretions.
. Extreme fatigue - malaise - sore throat - fever - generalized maculopapular rash.
. Posterior cervical lymphadenopathy & palatal petichae.
. Splenomegaly is common.
. Contact sports sh'd be avoided to prevent splenic rupture.
. Leukocytosis with variant lymphocytes (Atypical lymphocytes).
. Dx -> HETEROPHIL ANTIBODIES (SENSITIVE & SPECIFIC).
. HETEROPHIL ANTIBODIES may be NEGATIVE in EARLY disease.
. -ve HETEROPHIL ANTIBODIES doesn't exclude IM.
((IDIOPATHIC IMMUNE THROMBOCYTOPENIA (ITP)))
Check for hepatitis C & HIV infections.
HCV & HIV tests as ITP may be the initial presentation of HIV infection
((SENILE PURPURA))
. occurs in areas susceptible to traumas in elderly (Dorsum of the hands & forearms).
. Due to PERIVASCULAR CONNECTIVE TISSUE ATROPHY .
. Lesions rapidly resolve leaving a brownish discoloration from hemosiderin deposition.
. Requires no ttt.
((HEPARIN INDUCED THROMBOCYTOPENIA (HIT)))
. TTT is started on clinical suspicion before serotonin assay.
((WARFARIN INDUCED SKIN NECROSIS))
. More common in females.
. Common sites: breasts , buttocks, thighs & abdomen.
. Initial complaint is PAIN FOLLOWED BY BULLAE FORMATION & SKIN NECROSIS.
. Occurs within weeks after starting therapy.
. Tx -> Discontinue warfarin - Give heparin to continue anticoagulation - Give Vit. K.
. Acetaminophen, NSAIDs & Amiodarone may potentiate the anticoagulant effect of warfarin.
((VITAMIN K DEFECIENCY BLEEDING))
. Pt kept NPO (NOTHING PER ORAL) for a prolonged period of time & receiving Antibiotics.
. OR Newborn hadn't received prophylactic vit. K (Home-born) for prevention of hemorrhage
. ++++ PT > ++ PTT.

((HYPOCALCEMIA MANIFESTATIONS (PARESTHESIA) AFTER BLOOD TRANSFUSION))
. Occurs in pts who receive more than one blood volume of blood transfusion or packed RBCs over 24 hours may develop ++ plasma level of CITRATE (A SUBSTANCE ADDED TO STORED BLOOD) -> CHELATION of Ca & Mg by citrate -> -- Ca -> Paresthesia.
((MIGRATORY SUPERFICIAL THROMBOPHLEBITIS = TROUSSEAU's $YNDROME))
. Hypercoagulable disorder.
. Un-explained superficial venous thrombosis at un-usual sites e.g. arm & chest area.
. Associated with OCCULT VISCERAL MALIGNANCY !
. Ex. Cancer involving the pancreas "most common".
. The tumor releases mucin that react with platelets forming platelet rich micro-thrombi.
. H/O of heavy smoking - abdominal pain - migrattory thrombophlebitis.
. Dx -> CT Abdomen -> searching for an occult tumor (pancreatic carcinoma).
((GLUCAGONOMA))
. Necrolytic migratory erythema:
-> Erythematous papules / plaques on face, perineum & extremities.
-> Enlarge & coalesce with central clearing & blistering & crusting & scaling.
. Diabetes Mellitus:
-> Mild hyperglycemia easily controlled with diet & oral agents.
-> Don't require insulin !
. GIT symptoms:
-> Diarrhea - anorexia abdominal pain - occasional constipation.
. Other findings:
-> Weight loss.
-> Neuropsychiatric (ataxia - dementia - proximal ms weakness).
-> Associated wih venous thrombosis !
. Dx -> Hyperglycemia with ++ GLUCAGON > 500 mg/dl.
. Dx -> Normocytic Normochromic anemia.
. Dx -> CT or MRI to detect the tumor.
((SMOKER + HORNER's $ = LUNG CANCER))
. Horner's $ -> Miosis, ptosis & anhydrosis.
. Simple CXR is the best next step to detect lung cancer.
((SMALL CELL (OAT) LUNG CARCINOMA))
. Associated with $yndrome of inappropriate ADH secretion & ACTH production.
. SIADH (Hyponatremia & -- serum osmolality & ++ urine osmolality).
. Metastasis is already present at the time of diagnosis !
. Tx of SIADH -> Mild (Fluid restriction) or Severe (Hypertonic saline).
. ++ ACTH -> Hypertension - Hypokalemia - Metabolic alkalosis - Hyperpigmentation.
. e'out other manifests of Cushing $ (Moon face - Dorsal hump - central obesity - striae)
((SQUAMOUS CELL CARCINOMA OF THE LUNG))
. Significant smoking H/O.
. HYPERCALCEMIA ++ Ca -> (sCa++mous) !
. Hilar mass.
((ADENOCARCINOMA OF THE LUNG))
. Least association with smoking.
. Located peripherally.
. Consists of columnar cells growing along the septa.
. Presents as a sloitary nodule !
. May be detected incidentally.
((FEBRILE NEUTROPENIA))
. Single temperature > 38.3c or sustained temp. > 38 c for > 1 hour in a neutropenic pt.
. Neutropenia = Absolute neutrophil count < 1500 cells/ml.
. Mild ( PAN-ENDOSCOPY.
. Tx -> Radical neck dissection.
((TESTICULAR TUMOR))
. Painless hard mass in testicle.
. Suggestive ultrasound.
. Tx -> Orchiectomy (Removal of the testicle & its associated cord).
. FNAC or trans-rectal biopsy are contr'd bec. the risk of spillage of cancer cells.

((FIBROCYSTIC DISEASE OF THE BREAST))
. Rubbery, firm, mobile & painful mass in a young pt.
. More pain during menses.
. Aspiration of the cyst -> Clear fluid with diasppearance of the mass.
. Tx -> Observation of the pt 4 - 6 weeks.
. Only send the fluid for cytology if there is blood or foul smelling.
((INVASIVE DUCTAL BREAST CARCINOMA))
. TNM staging is the single most important prognostic tool for breast cancer.
. Prognosis is best detected using ONCOGENE AMPLIFICATION by FISH !
. FISH = Fluorescent in situ hybridization.
. Over-expression of the oncogene HER2 can be detected by FISH = (Worse prognosis).
. Positivity predicts a +ve response to TRASTUZUMAB & ANTHRACYCLINE chemotherapy.
. ER +ve & PR +ve are GOOD prognostic features.
. Tx -> TRASTUZUMAB (Herceptin) is used to ttt breast cancer that is HER2 +ve.
. Trastuzumab side effect -> CARDIOTOXICITY.
. ECHOCARDIOGRAPHY is recommended before ttt to assess the ejection fraction.
((INFLAMMATORY CARCINOMA OF THE BREAST))
. Breast cancer sh'd be considered whenever a pt. without a prior H/O of skin disease develops a breast rash that is non-responsive to standard ttt !
. When invasive ductal carcinoma is severe, it can infiltrate into the dermal lymphatics resulting in edema - erythema - warmth of the entire breast (inflammatory carcinoma).
. When the rash is localized to the nipple & has an ulcerating eczymatous appearance the primary cosideration should be PAGET's DISEASE of the breast.
. 5 % of pts with PAGET's disease have an underlying breast cancer "ADENO-CARCINOMA".
. Skin biopsies -> large cells surrounded by clear halos == PAGET’s.

((TAMOXIFEN))
. Has mixed agonist & antagonist activity on Estrogen receptors.
. It is used as an adjuvant therapy for early stage breast cancer,
. It reduces the risk of recurrence of the original cancer,, BUT,, ++ risk of developing of another cancer in the other breast !
. Estrogenic effects ++ risk of ENDOMETRIAL cancer & Venous thrombosis.
((SQUAMOUS CELL CARCINOMA of the SKIN))
. Any scar that develops into a non-healing, painless, bleeding ulcer.
. Sun-exposed or burned areas are typically involved.
. Rough scaly nodules that can ulcerate & metastasize.
. Tar derivatives (tobacco smoke) & chronic radiation exposure are predisposing factors.
. Dx -> PUNCH BIOPSY.
. Tx -> Surgical removal with wide excision of the skin around the tumor.
((BASAL CELL CARCINOMA of the SKIN))
. Most common form of skin cancers in USA.
. Open sore that bleeds, oozes or crusts & remains open for 3 or more weeks.
. Reddish patch or irritated area, shiny, waxy, scar like with elevated rolled borders.
. Remains local - Never spreads.
. Tx -> Mohs surgery (Microscopic shaving) -> 1-2 mm of clear margins are excised.
. Highest cure rate with Mohs surgery.
. Indicated in lesions located at critical areas e.g. perioral region, nose, lips & ears.
((ESOPHAGEAL CARCINOMA))
. Heart burn - significant weight loss - Regurgitation of food - fatigue - smoking H/O.
. Age > 50 ys.
. Histological types -> Squamous cell carcinoma & Adenocarcinoma.
. SCC -> Ass. with smoking & alcohol consumption.
. Adenocarcinoma -> Barret's esophagus (GERD complication).
. Dx -> BARIUM SWALLOW followed by ENDOSCOPY.
((MYASTHENIA GRAVIS))
. Ptosis & double vision by the end of the day.
. Dx -> EMG -> Decremental response in compound action potential.
. Dx -> Acetyl choline receptor antibody test +ve.
. Dx -> CT scan chest sh'd be done in all newly diagnosed MG pts searching for a THYMOMA.
((COLON CANCER SCREENING))
* ROUTINE:
-> Colonoscopy at 50 ys then every 10 ys.
* SINGLE FAMILY MEMBER WITH COLON CANCER:
-> Colonoscopy at 40 ys,
-> or .. 10 ys earlier than the age at which the family member had cancer,
-> whichever is earlier then every 10 ys.
* HNPCC 3 family members & 2 generations & 1 premature (90%) -> parathyroid hyperplasia -> primary hyperparathyroidism -> ++ Ca.
. Pituitary -> prolactinoma.
. Pancreas / GIT -> Gastrinoma "ZE $" - insulinoma - VIPoma - Glucagonoma.
. KEY WORDS-> INTRACTABLE ULCERATION + HYPERCALCEMIA -> ZE$ & Hyperparathyroidism = MEN1.
((POST-SPLENECTOMY SEPSIS))
. Asplenic pt have defective PHAGOCYTOSIS !
. Impaired antibody mediated opsonization in phagocytosis.
. High risk of overwhelming infection by encapsulated organisms,
. e.g. Strept. pneumoniae, N. menengitidis & H. influenzae.
((DEEP VENOUS THROMBOSIS = DVT MANAGEMENT))
. Presents with pain, swelling & discoloration.
. D.D. -> Ruptured Baker's cyst - venous insuffeciency - post-thrombotic $ & cellulitis.
. Failure to anti-coagulate the pt may lead to pulmonary embolism.
. Modified Wells criteria is a pretest propability of DVT:
-> Previous DVT.
-> Active cancer.
-> Recent immobilization.
-> Localized tendrness along vein distribution.
-> Swollen leg.
-> Pitting edema.
. Pre-test propability of DVT using WELLs criteria
.|
.| .|
. Not likely . Likely
| .|
. D-Dimer test (+) >. Compression Ultrasonography
.| .|
.| .________________ _____________________
.| .| .|
(-) (+) (-)
.| .| .|
. Un-likely to have DVT ! (TTT with Heparin & Warfarin) (Contrast Venography)
((Clinical features of METASTATIC BRAIN CANCER))
. Incidence -> Lung > Breast > Un-known primary > Melanoma > Colon.
. Primary solitary brain metastases -> BREAST - COLON - RENAL CELL CARCINOMA.
. Multiple brain metastasis -> LUNG - MALIGNANT MELANOMA.
. Brain metastasis is the most common intracranial tumors.
. Headache – nausea & vomiting - seizures & focal neurological symptoms (weakness-aphasia).
((TYPES OF THERAPIES))
. ADJUVANT -> TTT given in addition to standard therapy.
. INDUCTION -> Initial dose of ttt to rapidly kill tumor cells.
. CONSOLIDATION -> TTT given after induction therapy to -- the tumor burden.
. MAINTENANCE -> Given after induction & consolidation ttt to kill residual tumor cells.
. NEO-ADJUVANT -> Given before the standard therapy for a particular disease.
. SALVAGE -> TTT for a disease when the standard ttt fails.
((MECHANISM OF ACTION of IMP. DRUGS))***IMP***
. HEPARIN -> "Anti-coagulant" -> ++ ANTI-THROMBIN 3 -> -- Thrombin, 9 & 10.
. WARFARIN -> "Anti-coagulant" -> -- synthesis of Vit. K dep. factors 1972, ptn C & S.
. ASPIRIN -> "Anti-platelet" -> -- cyclo-oxygenase 1 -> -- TXA 2 synthesis.
. CLOPIDOGREL ->"Anti-platelet" -> block platelet surface receptors -> -- platelet activ.
((ANDROGEN ABUSE))
. Athletes commonly abuse androgen to enhance performance in competitive sports.
. Ex: testosterone & synthetic androgen.
. ++ Muscle mass & strength & ++ physical exercise intolerance.
. Men SEs -> -- testicular function - -- sperm production - testicular atrophy.
. Men SEs -> Gynecomastia - mood disturbance - aggressive behavior.
. Women SEs -> ++ Acne - Hirsutism - deepening of voice - menstrual irregularities.
. Labs -> Erythrocytosis & ++ HCT - Hepatotoxicity - Dyslipidemia ( -- HDL & ++ LDL).
((SOLITARY PULMONARY NODULE APPROACH))
. 3 cm or less coin-shaped lesion,
. in the middle to lateral one third of the lung.
. Surrounded by normal parenchyma.
. Most of them are benign !
. Calcifications of the nodule favors a benign lesion !
. POP CORN calcification -> Hamartoma.
. BULLS EYE -> Granuloma.
. Low risk pts (< 40 ys & non smokers) -> Not a sign of immediate alarm.
. Best approach -> ASKING FOR AN OLD X-RAY !
. If no change in it for the last 12 months -> Benign.
. Followed by CXR every 3 months for the next 12 months -> If no growth or syms -> Leave!
. High risk pts (> 40 ys & smokers) -> Full investigation work up !
((GIANT CELL TUMOR OF BONE))
. Dx -> X-ray -> Expansile & eccentric lytic area with SOAP & BUBBLE APPEARANCE.
. Benign but locally aggressive skeletal neoplasm.
. Young adults.
. pain, swelling & -- range of motion at the involved site.
. Pathologic #s are common due to thinning of the bone cortex in weight bearing areas.
. Affect the epiphysis of the long bones (distal femur & proximal tibia).
. MRI -> Tumor containing both cystic & hemorrhagic regions.
. Tx -> Surgery.
((COMPRESSION OF THE THECAL SAC or SPINAL CORD by a TUMOR))
. Ex -> H/O of prostatic cancer + Acute onset back pain.
. Rapid recognition is crucial to avoid paralysis.
. Point tenderness over the spine process L5 & S1.
. Imbalance, ms weakness & week rectal sphincter tone.
. Dx -> MRI spine BUTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTTT
. Initial management with glucocorticoids (dexamethasone) is crucial to -- swelling,
. as an attempt to preserve neurological function while awaiting the results of imaging.
((POST-SPLENECTOMY RECOMMENDATIONS))
. Risk for sepsis after splenectomy is present UP TO 30 years & more !
. Anti-pneumococcal, Haemophilus & meningococcal vaccine sh'd be given,
. several weeks before splenectomy.
. Daily oral penicillin prophylaxis for 3 - 5ys following splenectomy.

((CANCER OVARY))
. NO screening tests !
. Serum CA 125 & pelvic U/$ may help in diagnosis.
((++ HOMOCYSTEINE levels -> HYPERCOAGULABILITY))
. Vit. B6, Folate & Vit. B12 are involved in the metabolism of homocysteine.
. Vit. B6 lowers homocysteine levels by acting as a cofactor for cystathionine B-synthase
. which metabolizes homocysteine to cystathionine.
((PAIN CONTROL IN CANCER PATIENTS))
. Give the appropriate pain medication to cancer pts e.g. Ibuprofen.
. If no response .. Use a narcotic drug if it is the most appropriate.
. Use SHORT ACING IV MORPHINE.
((MANAGEMENT OF CHEMOTHERAPY INDUCED NAUSEA & VOMITING))
. Volume repletion + SEROTONIN ANTAGONIST (Block 5HT3 recptors).
((MANAGEMENT OF CANCER RELATED ANOREXIA & CACHEXIA))
. PROGESTERONE ANALOG -> ++ Appetite & ++ weight gain.
((PROSTATE CANCER with BONE METASTASIS))
. Tx -> FOCAL EXTERNAL BEAM RADIATION (If the pt under-went orchiectomy !).
((BRAIN METASTASIS))
. SOLITARY -> SURGICAL RESECTION followed by whole brain radiation.
. Multiple -> Palliative whole brain radiation.
((MANAGEMENT OF HYPERCALCEMIA DUE TO UNDERLYING MALIGNANCY))
. Asymptomatic or mild -> Ca < 12 mg/dl:
. Just avoid thiazides, lithium use, volume depletion or prolonged bed rest.
. Severe -> Ca > 14 mg/dl:
. Immediate ttt -> Normal saline hydration + Calcitonin.
. Long term ttt -> Biphosphonate (Zoledronic acid).
((D.D. of ANTERIOR MEDIASTINAL MASS (4 Ts)))
. Thymoma - Teratoma - Thyroid neoplasm - Terrible lymphoma.
. Germ cell tumors are classified into seminomatous & non-seminomatous.
. Non-seminomatous (Yolk sac tumor - choriocarcinoma - embryonal carcinoma).
. A mixture of all types of non seminomatous germ cell tumors = MIXED GERM CELL TUMOR.
. Seminoma -> ++ B-HCG & Normal AFP.
. Non seminoma (MIXED) -> ++ B-HCG & ++ AFP.
((HEMOCHROMATOSIS))
. NEW-ONSET DIABETES MELLITUS + ARTHROPATHY + HEPATOMEGALY.
. Due to abnormal ++ intestinal absorption of iron -> ++ iron deposition in tissues.
. Damage to organs ex. liver, pancreas , heart & pituitary.
. Liver -> Hepatomegaly -> Liver cirrhosis -> Hepatocellular carcinoma.
. Pancreas -> Bronze D.M.
. Pituitary -> Hypogonadism.
. Heart -> Restrictive heart failure.
. Joints -> Arthropathy.
. Skin -> Hyperpigmentation.
. Dx -> Iron studies -> ++ fe, ++ ferritin, ++ transferrin saturation.
. Dx -> Liver biopsy -> confirm the diagnosis.
((LEAD POISONING))
. Lead bind to erythrocytes & disrupts hemoglobin synthesis -> Microcytic anemia.
. Due to chronic lead exposure & toxicity.
. Acute exposure -> Abdominal pain & constipation.
. Chronic exposure -> Fatigue, iiritability & insomnia.
. Hypertension - Sensori-motor neuropathies - Neuropsychiatric disturbances - Nephropathy
. OCCUPATIONAL HISTORY IS VERY IMPORTANT !
. BATTERY MANUFACTURING - PLUMBING - MINING - PAINTING - PAPER HANGING & AUTO-REPAIR.
. Dx -> Blood Lead level.
. Dx -> Peripheral smear -> BASOPHILIC STIPPLING.
. Tx -> CHELATION THERAPY.
=====================================================================================
ENDOCRINOLOGY
((HASHIMOTO's THYROIDITIS))
. Anti-TPO Abs (Anti-thyroid peroxidase antibodies).
. High risk of developing THYROID LYMPHOMA.
((GENERALIZED RESISTANCE to thyroid hormones))
. ++ T3 & T4 levels.
. ++ or Normal TSH level.
. features of HYPO-thyroidism despite having ++ free T3 & T4.
((SICK EUTHYROID $YNDROME = LOW T3 $YNDROME))
. Abnormal thyroid function tests with an acute severe illness.
. May be due to caloric deprivation.
. Fall in total & free T3 levels with NORMAL T4 & TSH. !!!
((FACTITIOUS THYROTOXICOSIS))
. Due to exogenous thyroid hormone.
. H/O of psychiatric illness or attempted weight loss (Herbal remedy!).
. Thyrotoxicosis syms (Palpitations - sweating - weight loss - hyperactivity & diarrhea).
. Lid lag may be present but NO exophthalmos (Excluding Grave's dis.).
. The ingested thyroid hormone disturbs the native thyroid axis !
. RAIU is decreased (-- Radio Active Iodine Uptake).
. Dx -> "LOW SERUM THYROGLOBULIN" is the main stay of diagnosis.
. Dx -> -- TSH & ++ T3 &/or T4.
((THYROID RADIOACTIVE IODINE SCAN))
. HASHIMOTO's THYROIDITIS -> Heterogenous pattern.
. GRAVE's DISEASE ---------> Diffusely ++ uptake.
. MULTINODULAR GOITER -----> PATCHY.
. PAINLESS THYROIDITIS ----> -- markedly reduced uptake.

((SIDE EFFECTS OF RADIO-IODINE THERAPY -> HYPO or HYPER thyroidism !!))
.HYPOTHYROIDISM:
. Destruction of thyroid follicles by radioactive iodine.
. Tx of hypothyroidism is Levo-thyroxine.
. Ophthalmopathy may worsen in 10 % of cases.
. THYROTOXICOSIS:
. may be a side effect of RADIO-IODINE therapy !!
. I - 131 is taken up by thyroid follicles & then destroys them by emitting B-rays.
. Dying thyroid cells may release excess thyroid hormone into the circulation.
. Aggravating the hyperthyroid state.
((CONTRA-INDICATIONS to RADIO-ACTIVE IODINE THERAPY))
. PREGNANCY.
. VERY SEVERE OPHTHALMOPATHY.
((SIDE EFFECTS of ANTI-THYROID DRUGS (PROPYLTHIOURACIL)))
. AGRANULOCYTOSIS (fever & sore throat) -> Stop the drug !
((SURGERY SIDE EFFECTS))
. Permanent hypothyroidism.
. Risk of recurrent laryngeal nerve damage.
((COMPLICATIONS of UN-TREATED HYPER-THYROID PATIENTS))
-> RAPID BONE LOSS -> due to ++ osteoclastic activity .
-> CARDIAC TACHYARRHYTMIA (AF).
((HYPERTENSION in pts with THYROTOXICOSIS))
. is predominantly SYSTOLIC.
. caused by HYPERDYNAMIC CIRCULATION.
((INDICATIONS OF THYROID FUNCTION TESTS))
-> HYPERLIPIDEMIA.
-> Un-explained hyponatremia.
-> Un-exlained ++ CPK.
((THYROID MALIGNANCIES))
1 * PAPILLARY CARCINOMA:
-> MOST COMMON TYPE & BEST PROGNOSIS.
-> Slow infiltrative local spread.
-> Presence of PSAMMOMA bodies.
2 * MEDULLARY CARCINOMA:
-> CALCITONIN secretion.
3 * FOLLICULAR CARCINOMA:
-> Invasion of the tumor capsule & blood vessels.
-> Early metastasis to distant organs.
((BIOCHEMISTERY IMPORTANT INFO))
. GLUCONEOGENESIS main substrates:
. Alanine - Lactate - Glycerol 3 phosphate.
. PYRUVATE is an INTERMEDIATE of Alaninie.
((MULTIPLE ENDOCRINE NEOPLASIA (MEN)))
* MEN TYPE 1:
. Parathyroid adenoma.
. Pituitary tumor.
. Pancreatic tumor.
. {Mutation in the MEN 1 tumor suppressor gene}.
* MEN TYPE 2A:
. Medullary thyroid cancer (HARD NODULE - ++ Calcitonin - Malignant cells on FNAB).
. Pheochromocytoma.
. Parathyroid hyperplasia.
. Less aggressive (No associated cancers).
* MEN TYPE 2B:
. Medullary thyroid cancer (HARD NODULE - ++ Calcitonin - Malignant cells on FNAB).
. Pheochromocytoma (++ urinary metanephrines & nor-epinephrines levels).
. Neuromas (mucosal & intestinal).
. Marfanoid habitus (-- upper to lower body ratio - hypermobile joints - scoliosis).
. {Mutation in the RET proto-oncogene located on chromosome 10}.
. DNA testing is used for screening.
. More aggressive (Associated cancers).
((DM SCREENING TESTS))
.1. GLYCOSYLATED HEMOGLOBIN Hb A1C:
. It is used to monitor chronic glycemic control.
. It is reflective of the pt's average glucose levels over the past 100-120 days.
. Preferred test in non fasting state.
. > 6.5 -> DM.
. < 5.7 -> Normal.
.2. FASTING BLOOD GLUCOSE:
. No caloric intake for 8 hours.
. > 126 mg/dl -----> DM.
. 100 - 125 mg/dl -> Impaired fasting glucose.
. 70 - 99 mg/dl ---> NORMAL.
.3. RANDOM GLUCOSE LEVEL:
. > 200 mg/dl with symptoms of hyperglycemia.
.4. ORAL GLUCOSE TOLERANCE TEST:
. MOST SENSITIVE TEST.
. 75 g glucose load with glucose testing for 2 hours.
. > 200 mg/dl -----> DM.
. 140 - 199 mg/dl -> Impaired glucose tolerance.
((DKA DIABETIC KETOACIDOSIS))
. Blood glucose level > 250.
. pH < 7.3
. Low serum HCO3 < 15-20
. Detection of plasma ketones.
. ++ ANION GAP {(Na) - (Cl+HCO3)} ----> AG > 8-12.
. H/O of previous stressor e.g. recent GIT infection.
. H/O of weight loss, ployurea & polydipsia.
. Deep rapid breathing (Kussmaul's respiration).
. Osmotic diuresis -- total body K (But : Serum K may be elevated!).
. ++ in K level due to EXTRA-CELLULAR SHIFT.
. PARADOXICAL HYPERKALEMIA (The body potassium reserves are actually depleted!)
. 1st initial simple step to detect DKA --> FINGER-STICK GLUCOSE !

((DKA MANAGEMENT))
.1. RAPID INTRAVENOUS NORMAL SALINE (0.9% SALINE).
.2. RAPID INTRAVENOUS REGULAR INSULIN.
.3. K correction.
.4. TTT of infections e.g. Abs.
. ARTERIAL pH or ANION GAP is the most reliable indicator of metabolic recovery in DKA.
((HYPER-GLYCEMIC HYPER-OSMOLAR NON-KETOTIC COMA))
-> Very high glucose levels.
-> Very high plasma osmolality.
-> NORMAL ANION GAP.
-> NEGATIVE SERUM KETONES.
((Non ketotic - Hyperglycemic coma management))
. Fluid replacement with NORMAL SALINE.
((Comparison))***IMP***
. DIABETIC KETOACIDOSIS (DKA) .................... HYPEROSMOLAR HYPERGLYCEMIC STATE
. Type (1) DM usually. ____________________ . Type (2) DM.
. YOUNGER age. ____________________ . Older.
. LESS confusion. ____________________ . MORE confusion.
. Hyperventilation MORE common _____________ . Less common.
. Abdominal pain MORE common. ___________ . LESS common.
. Glucose 250 - 500 mg/dl. ___________________ . > 600
. HCO3 < 18 meq/L. ____________________ . > 18
. +++++ ANION GAP. ____________________ . NORMAL.
. POSITIVE serum ketones. __________________ . NEGATIVE.
. Serum osmolality < 320 _________________ . > 320.
((DIABETIC NEPHROPATHY))
. Begins with HYPERFILTRATION (++GFR) & MICROALBUMINURIA.
. If not ttt well .. Micro becomes Macroalbumiuria > 300 mg/dl.
. INTENSIVE BLOOD PRESSURE CONTROL to prevent worsenening of the condition.
. Use ACE Is with blood pressure goal 130/80 mmHg.
. Most sensitive screening test is -> RANDOM URINE MICRO-ALBUMIN/CREATININE RATIO.
((DIABETIC NEUROPATHY))
. DISTAL SYMMETRIC SENSORIMOTOR PLOYNEUROPATHY.
. STOCKING GLOVE pattern.
. It is the most common risk factor of foot ulcerations in diabetics.
. Tx -> TCAs (Amitriptyline - Gabapentin).
((DIABETIC GASTROPATHY))
. Autonomic neuropathy of the GIT.
. Symptoms of delayed gastric emptying & gastroparesis.
. -- Esophageal dysmotility -> Dysphagia.
. -- Gastric emptying -------> Gastroparesis.
. Gastroparesis (Nausea - vomiting - early satiety - postprandial fullness).
. -- intestinal function ----> diarrhea - constipation - incontinence.
. Tx -> DM control - SMALL FREQUENT MEALS - METOCLOPROMIDE (prokinetic & Antiemitic).
. SEs of Metoclopromide -> Extrapyramidal syms -> Tardive dyskinesia (Give Erythromycin).
((ERECTILE DYSFUNCTION in D.M))
. Due to vascular complications & neuropathy.
. 1st line of ttt is phosphodiesterase inhibitor (Sildenafil).
. Contr'd in pts being ttt with NITRATES.
. Sildenafil may predispose to PRIAPISM.
. When combined with an Alpha blocker (Prazosin), it is imp. to give them 4 hrs apart,,
. to avoid SEVERE HYPOTENSION.
.((DIABETIC FOOT management -> DEBRIDEMENT & proper wound care)).

((CAUSES OF HYPOGLYCEMIA in NON-DIABETIC pts))
1 - INSULINOMA (BETA cell tumor).
2 - SURREPTITIOUS use of insulin or sulfonylurea.
. INSULINOMA:
. BETA CELL TUMOR.
. Normally, blood glucose < 60 mg/dl result in complete suppression of insulin secretion.
. Hypoglycemia in the presence of inappropriately ++ serum insulin levels = insulinoma.
. ++ C-peptide level.
. ++ Pro-insulin.
((DIABETES INSIPIDUS))

. Due to ADH defeciency or resistance.
. Urine osmolality is < serum osmolality.
. Polyurea & polydipsia.
. H/O of tendency to COLD BEVERAGES to QUENCH THIRST.
. Exclude psychogenic polydipsia using water deprivation test.
. Differentiate bet. central & nephrogenic DI using ARGININE VASOPRESSIN.
. Tx -> NORMAL SALINE.
. Tx -> CENTRAL -> INTRANASAL SPRAY DDAVP.
. Tx -> NEPHROGENIC -> NSAIDs & HCZ.

((HOW CAN U DIFFERENTIATE BET. DI & PSYCHOGENIC POLYDIPSIA))
. WATER DEPRIVATION TEST:
. Failure to concentrate urine after deprivation -> DI.
. Production of concentrated urine ---------------> Psychogenic polydipsia.
((HOW CAN U DIFFERENTIATE BET. CENTRAL & NEPHROGENIC DI))
. ARGININE VASOPRESSIN (AVP) or DESMOPRESSIN adminstration:
. CENTRAL DI -----> ++ in urine osmolality.
. NEPHROGENIC DI -> No significant ++ !
((SYNDROME OF INAPPROPRIATE ADH SECRETION (SIADH)))
. ++ ADH levels without stimuli of its release.
. NORMAL SERUM osmolality -> 275 - 295 mOsm.
. NORMAL URINE osmolality -> 50 - 1400 mOsm.
. Dx -> Simultaneous measurment of urine & plasma osmolality.
. The normal response to hypotonicity (low plasma osmolality) is the production of maximally diluted urine (low urine osmolality -> < 100 mOsm.)
. LOW plasma osmolal. (100-150mOsm) is diagnostic.
. Tx of SIADH:
-> Mild symptoms (forgetfulness & unstable gait) -> Fluid restriction.
-> Moderate symptoms (Confusion & lethargy) -> HYPERTONIC SALINE (3%).
-> Severe symptoms (seizures & coma) -> Hypertonic saline + Conivaptan.
SO : CCC (confusion/convulsion/coma) = hypertonic saline
((BOTTOM LINE))
* Diabetes insipidus:
. Polyurea - polydipsia - excretion of diluted urine with ++ serum osmolality.
* 1ry (Psychogenic) polydipsia:
. Excessive water drinking -> BOTH plasma & urine are diluted.
* SIADH:
. Hyponatremia - LOW serum osmolality & inappropriately high urine osmolality.
((P.O.C. ------- # DIABETES INSIPIDUS -------- # PSYCHOGENIC POLYDIPSIA ------ # SIADH))
_____ __________________ ______________________ _____
-> SERUM osm. ---> (+) (-) (-)
-> URINE osm. ---> (-) (-) (+)

((ANDROGEN PRODUCING ADRENAL TUMOR in FEMALES))
. Best indicator is DHEA-S = De-Hydro Epi-Androsterone Sulfate.
(( ++ Ca (Hyperclacemia) Approach)) -> Measure Parathormone (PTH):
* ++ Ca & ++ PTH -> 1ry hyperparathyroidism (abd. groans - renal stones - bones - moans).
* ++ Ca & -- PTH -> Malignancy - vit. D toxicity - Sarcoidosis.
-- Ca & ++ PO4 causes -> CRF & Primary hypothyroidism.
((CHRONIC RENAL FAILURE))
. -- Ca & ++ PO4 & ++ PTH.
. Exclude CRF by NORMAL renal function tests (urea & creatinine).
((Causes of ++ Ca & + PTH: 1ry Hyperparathyroidism & familial hypocalciuric hypercalcemia))
. Differentiated by 24 hour urinary calcium:
. Primary Hyper-parathyroidism ---------> > 250 mg.
. Familial hypocalciuric hypercalcemia -> < 100 mg.
((PRIMARY HYPER-PARA-THYROIDISM))
. Causes -> Parathyroid adenoma (90%) - hyperplasia (6%) & carcinoma (2%).
. Associated with MEN 1 & 2A.
. 80 % of pts are asymptomatic.
. Abdominal groans, renal stones, bones #s & psychic moans.
. ++ Ca & -- PO4 & ++ or normal PTH.
. 24 hours urinary calcium > 250 mg.
. Urinary calcium/creatinine > 0.02 (To rule out familial hypo-calciuric hyper-calcemia).
. Dx -> 3Ds SESTAMIBI scan + U/$ to locate the hyperactive parathyroid tissue pre-surgery.
. Tx -> Parathyroidectomy for symptomatic pts.
((Surgery indications))
-> Serum Ca level > 1 mg/dl above the upper limit of normal (11mg/dl).
-> Young age < 50 ys.
-> Bone mineral density < T-2.5 at any stage.
-> -- Renal function (GFR < 60ml/min.).
((HYPERCALCEMIA of MALIGNANCY))
. ++ Ca -> confusion - lethargy - fatigue - anorexia - polyuria & constipation.
. Associated with SQUAMOUS cell lung cancer.
. CXR finding of lung cancer (lobar mass & perihilar lymphadenopathy).
. Malignancy produces PTH related peptide PTHrP -> ++ Ca & -- PO4.
((HYPERCALCEMIA (++Ca) ALGORITHM))
(++Ca)
.|
.Measure PTH level
.|
.| .|
.(+++) .(---)
.(PTH dependent) . (PTH-INdependent)
.| .|
.Measure urinary Ca _______________________________________
.| .| .| .| .|
.________________ .+PTHrP .+1,25(OH)D .+25(OH)D .NORMAL LABs
.| .| .| .| .| .|
.> 250 .< 100 .TUMOR .Lymphoma-Sarcoid . Vit.D toxicity .HYPERTHYROIDISM
.| .| .MULTIP MYELOMA
1ry or 3ry .Familial .Adrenal tumor
Hyperpara- .Hypercalcemic .Acromegaly
thyroidism .Hypocalciuria .Vit.A toxicity
.Immobilization
((IMPORTANT CASE SCENARIO))
. Rapid ascend to a height of 10000 feet -> HYPO-calcemia ! HOW ?? (++ Albumin bound Ca).
. Respiratory alkalosis = ++ pH level -> ++ the affinity of serum albumin to calcium.
. ++ the levels of ALBUMIN-bound Ca -> -- the level of IONIZED Ca (Active form).
. -- Ionized Ca (Active form) -> Hypocalcemia manifestations.
((ACTH defeciency (2ry adrenal insuffeciency): "-- Glucocorticoids"))
-> Postural hypotension & tachycardia.
-> Fatigue & weight loss.
-> -- libido, hypoglycemia & eosinophilia.
N.B: no hyperkalemia /no salt wasting/-- in skin pigmentation (KAPLAN)
((OSTEOPOROSIS))
. Postmenopausal woman.
. presenting with multiple bony #s.
. NORMAL serum Ca - PO4 & PTH & ALP.

((OSTEOMALACIA))
. Vit. D defeciency in ADULTS.
. Bony pain & tendrness.
. -- serum Ca & PO4.
. -- urinary Ca.
. ++ ALP & ++ PTH.
. -- 25 OH-D.
. X-ray -> BILATERAL SYMMETRIC PSEUDO-FRACTURES (LOOSER ZONES).
((PAGET's DISEASE))
. NORMAL serum Ca - PO4 & PTH.
. INCREASED ++ ALKALINE PHOSPHATASE.
. Tx -> BIPHOSPHONATES -> inhibit OsteoCLASTs asctivity.

Condition Calcium
Phosphate
Alkaline phosphatase
Parathyroid hormone
Comments
Osteoporosis unaffected unaffected normal unaffected decreased bone mass
Osteopetrosis
unaffected unaffected elevated unaffected thick dense bones also known as marble bone
Osteomalacia and rickets
decreased decreased elevated elevated soft bones
Osteitis fibrosa cystica
elevated decreased elevated elevated brown tumors
Paget's disease of bone
unaffected unaffected elevated unaffected abnormal bone architecture

((PATHOLOGY of bone diseases))
. OSTEOMALACIA -> -- Mineralization of the bone.
. RICKETS ------> -- Mineralization of the bone & CARTILAGE.
. PAGET's ------> Disordered remodeling.
. OSTEOPOROSIS -> NORMAL mineralization but low bone mass.
((CAUSES of HYPOKALEMIA & --BICARBONATE HCO3 {Metabolic Alkalosis} & high aldosterone)) -> (Check RENIN):
.. CAUSES of HYPOKALEMIA & ++ ALDOSTERONE & -- RENIN -> PRIMARY HYPER-ALDOSTERONISM.
.. CAUSES of HYPOKALEMIA & ++ BOTH ALDOSTERONE & RENIN -> (Check URINE Cl):
(A) WITH ++ URINE CHLORIDE (Check Na): (B) WITH -- URINE CHLORIDE:
1- -- Na -----> (Diuretic use). 1- Surreptitious vomiting.
2- Normal Na -> (Bartter's $). 2- Factitious diarrhea.
3- ++ Na -----> (Renin secreting tumor).
((SURREPTITIOUS VOMITING))
. Scars & calluses on the dorsum of the hands & dental erosions.
. Result from chemical & mechanical injury as the pt uses his hands to induce vomiting.
. Dental erosions result due to ++ exposure to gastric acid..
. May lead to hypovolemia & hypochloremia -> Low urine Cl level.
((CAUSES OF HYPERTENSION & HYPOKALEMIA))
. Primary hyperaldosteronism & Reno-vascular hypertension.
. Check the PLASMA RENIN ACTIVITY (PRA).
. Primary hyperaldosteronism -> LOW PRA.
. Reno-vascular hypertension -> HIGH PRA.
((PHEOCHROMOCYTOMA))
. Headache, palpitations, tremors, anxiety & flushing.
. Episodic elevations of blood pressue.
. Dx -> BEST INITIAL -> ++ catecholamines level in plasma & urine.
. Dx -> BEST INITIAL -> ++ metanephrines & VMA levels.
. Dx -> MOST ACCURATE -> CT or MRI or MIBG of the adrenal glands.
. Tx -> PHENOXYBENZAMINE (Alpha blocker) "FIRST" to control blood pressure.
. e'out Alpha blockage, BB may lead to CATASTROPHIC ++ in BP due to unopposed Alpha stim.
. Tx -> Propranolol is used "AFTER" an alpha blocker .
. Tx -> Surgical resection.
. N.B. It is a part of MEN type 2 A & B (DNA testing is imp. RET PROTO-ONCOGENE).
((CONGENITAL ADRENAL HYPERPLASIA ((CAH))
. ++ ACTH.
. -- Aldosterone & cortisol.
. Tx -> Prednisone.
. Types of CAH:
* 21 hydroxylase defeciency - * 11 hydroxylase defeciency - * 17 hydroxylase defeciency
* ++ Adrenal androgens - * ++ Adrenal androgens - * -- Adrenal androgens
* Hirsutism - * Hirsutism - * NO hirsutism
* ++ 17 hydroxy-progesterone - * NO - * NO
* NO hypertension - * HYPERTENSION - * HYPERTENSION
((LEYDIG CELL TUMORS))
. Most common type of testicular sex cord tumors.
. ++ ESTROGEN & -- FSH & LH.
((ANDROGEN SECRETING NEOPLASM of the OVARY or ADRENAL))
. Rapidly developing hyper-androgenism with verilization.
. Serum TESTOSTERONE & DHEAS levels are diagnostic.
. ++ TESTOSTERONE & NORMAL DHEAS -> OVARIAN source.
. NORMAL TESTOSTERONE & ++ DHEAS -> ADRENAL source.
((ERECTILE DYSFUNCTION))
. Failure to achieve a spontaneous erection.
. Causes:
. * NEUROGENIC -> injury of the parasympathetic nerve fibers (# pelvis or urethral tear).
. * VENOGENIC -> Disruption of tunica albuginea (# penis).
. * ENDOCRINOLOGIC -> ++ prolactin & -- Testosterone.
. * SITUATIONAL -> Anxiety (Nighttime & morning erctions are preserved).
((NOCTURNAL PENILE TUMESCENCE))
. helps to differentiate psychogenic from organic causes of male erectile dysfunction.
. +ve in psychogenic causes.
. -ve in organic causes.
=====================================================================================
DERMATOLOGY
((CELLULITIS))
. Generalized swelling which is erythematous "linear streaks", warm, tender but less well demarcated than Erysipelas.
((Tinea Corporis))
. Ring shaped scaly patches with central clearin & scaly borders.
. Dx: KOH -----> Hyphae. . Tx: Local Terbinafine or systemic Griseofluvin.
((Tinea Versicolor))
. Pale velvety pink or whitish hypopigmented macules that DON'T TAN !
. SCALE ON SCRAPING.
. Dx: KOH preparation ----> Spaghetti & meat ball appearance.
. Tx: Selenium sulfide.
((NECROTIZING FASCIITIS))
. Severe pain & swelling.
. H/O of recent trauma.
. High fever > 39 c.
. Edematous limb with PURPLISH DISCOLORATION of the injured area "denoting start of gangrene!".
. Surgical debridement of all necrotic tissue.
. Empiric IV Antibiotics e.g AMPICILLIN + SULBACTAM + CLINDAMYCIN.
. Bullae & seroanguinous discharge.
((PRIMARY BILIARY CIRRHOSIS))
. Pruritis, jaundice, steatorrhea, HSM, ++ ALP, ++ Bilirubin.
. +ve Anti-mitochondrial Antibodies.
. Immune mediated destruction of intra hepatic bile ducts ---> Bile stasis & cirrhosis.
. Cutaneous association ---> XANTHELASMA
."Yellowish, soft plaques on the medial aspects of the eyelids bilaterally".
((CHALAZION))
. Painful swelling that progress to a nodular rubbery lesion.
. due to MEIBOMIAN gland obstruction.
. Recurrent chalazion may be due to meibomian gland carcinoma !
. U can't differentiate bet. PERSISTENT CHALAZION & BASAL CELL CARCINOMA except through HISTOPATHOLOGICAL exam.
((MOLLUSCUM CONTAGIOSUM is caused by POX VIRUS))
((MELANOMA -----------> Excisional biopsy " FULL THICKNESS”))
((ANGIO-EDEMA))
. H/O of ICU pt on ACEIs e.g ENALAPRIL.
. Edema in the face, mouth, lips.
. Laryngeal edema may occur causing airway obstruction.
. occurs due to BRADYKININ release.
. it may occur at any time not just at the start of drug intake.
. Dx----> Low levels of C2 & C4.
. Tx----> STOP ACEIs + FRESH FROZEN PLASMA + Secure the airway.
((HERIDITARY angioedema))
. C1 esterase inhibitor defeciency.
((Drug induced PHOTOTOXICITY))
. The most common drug is DOXYCYCLINE (TETRACYCLINE).
. Manifest as exaggerated sunburn reactions with erythema ,edema & vesicles over sun- exposed areas.
((WARFARIN induced skin necrosis))
. More common in females.
. Common sites: Breasts, buttocks, thighs & abdomen.
. Initial complaint is pain followed by bullae formation & skin necrosis.
. Occurs within weeks after starting therapy.
. Tx: Discontinue WARFARIN & Give Vit. K & maintain anticoagulation using Heparin.
((ROSACEA))
. 30 - 60 ys old pt.
. TELANGECTASIA over the cheeks, nose & chin.
. Flushing of these area is precipitated by hot drinks, heat, emotion.
. Tx: initial ttt is METRONIDAZOLE.
Vitiligo ((Leukoderma))
. Young 20-30 ys.
. Pale whitish macules with hyperpigmented borders.
. Around body orifices.
. Auto-immine destruction of melanocytes.
((STEVENS JOHNS $YNDROME))
. Immune complex mediated hypersensitivity.
. H/O of SULFONAMIDES, NSAIDs & PHENYTOIN intake.
. Characteristic "TARGET" appearance.
. Fever, conjunctivitis, ++HR, --BP, altered consciousness, coma, convulsions may occur.
((RUBELLA))
. Middle aged female.
. Maculo-papular rash starting on the face & extends to involve the trunk & extremeties (Not involving the palms & soles).
. Tender lymphadenopathy (Post. auricular & post. cervical LNs).
. Poly-arthritis.
((Secondary $yhphilis))
. Maculopapular rash (involving the palms & soles).
. The papules may coalese to form CONDYLOMA LATA in severe cases!
((NICKEL jewelry can cause allergic contact dermatitis (Type 4 hypersensitivity)))
((Drug induced type 1 hypersensitivity reaction))
. IMMEDIATE ONSET.
. Mediated by IgE & Mast cells.
. Urticaria & pruritis without systemic symptoms.
. Tx: ANTI-HISTAMINICS & dis-continue the offending drug !
((The most concerning sign for malignancy in melanoma is ZONES OF DIFFERENT SKIN COLORS))
((SQUAMOUS CELL CARCINOMA))
. isolated solitary ulcer.
. in the Vermilion area of the lip.
. H/O of sun exposure (FARMER).
. Histologically: INVASIVE CORDS OF SQUAMOUS CELLS WITH KERATIN PEARLS.
((BASAL CELL CARCINOMA))
. INVASIVE CLUSTERS OF SPINDLE CELLS SURROUNDED BY PALISADED BASAL CELLS.
((CHERRY HEMANGIOMA))
. Small vascular bright red papular lesion.
. 30-40 ys & ++ in no with age "Senile hemangioma".
. Don't regress spontaneously.
. Sharply circumscribed areas of congested capillaries.
((ACTINIC KERATOSIS))
. Erythematous papule with a central scaling.
. Sand paper like texture.
. H/O of chronic sun exposure.
. Pre-cancerous ----> may convert to squamous cell carcinoma.
((Molluscum Contagiosum (Pox virus)))
. Firm, flesh colored, dome-shaped, umbilicated papules.
. Transmitted through sexual contact.
. Due to CELLULAR immunodefeciency.
. Associated with HIV.
((SHINGLES (HZV) may develop due to "INFLIXIMAB" therapy causing immunodeficiency))
((Allergic contact dermatitis))
. Type 4 hypersensitivity reaction.
. Prurutic erythematous rash with vesicles.
. Bilateral distribution.
. H/O of cutting woods (Poison Sumac).
. Vesicular fluid is sterile and grows coagulase -ve staphylococci (S. Epidermidis).
. May be 2ry infected staph or strept !
((ACANTHOSIS NIGRICANS))
. Symmetrical, hyperpigmented, velvety plaques in the axilla, groin & neck !
. Ass. with INSULIN RESISTANCE in YOUNG pts e.g. DM & PCO.
. Ass. with GIT malignancy in OLD pts.
==============================================================================
IMMUNOLOGY
((HYPER-SENSITIVITY REACTIONS))
{1} Type "1" (IMMEDIATE):
. Ex. Acute atopic dermatitis.
. Highly pruritic papules, vesicles & plaques.
. Light microscopy -> Spongiosis (edema of the epidermis).
Examples:
ƒ. Allergic and atopic disorders (eg, rhinitis, hay fever, eczema, hives, asthma)
ƒ. Anaphylaxis (eg, bee sting, some food/drug allergies)

{2} Type "2" (ANTIBODY MEDIATED):
. IgM or IgG + ANTIGEN.
. Ex. Immune hemolytic anemia & Rh hemolytic disease of the newborn.
Examples:
ƒ. Acute hemolytic transfusion reactions
ƒ. Autoimmune hemolytic anemia
ƒ. Bullous pemphigoid
ƒ. Erythroblastosis fetalis
ƒ. Goodpasture syndrome
ƒ. Graves disease
ƒ. Guillain-Barré syndrome
ƒ. Idiopathic thrombocytopenic purpura
ƒ. Myasthenia gravis
ƒ. Pemphigus vulgaris
ƒ. Pernicious anemia
ƒ. Rheumatic fever
{3} Type "3" (IMMUNE COMPLEX MEDIATED):
. Ag + Ab + COMPLEMENT.
. Ex. Serum sickness.
Examples:
ƒ. Arthus reaction
ƒ. SLE
ƒ. Polyarteritis nodosa
ƒ. Poststreptococcal glomerulonephritis
ƒ. Serum sickness
{4} Type "4" (CELL MEDIATED):
. Dermal inflammation after direct contact with allergen.
. Ex. Tuberculin skin test & Allergic contact dermatitis.
Examples:
ƒ. Contact dermatitis (eg, poison ivy, nickel allergy)
ƒ. Graft-versus-host disease
ƒ. Multiple sclerosis
((TRANSFUSION REACTIONS))
. 1 . ABO INCOMPATIBILITY:
. Acute symptoms of hemolysis WHILE the transfusion is occuring.
. Ex -> DURING a transfusion, the pt becomes hypotensive & tachycardic.
. Back & chest pain & dark urine.
. ++ LDH & bilirubin.
. -- Haptoglobin.
. 2 . TRANSFUSION RELATED ACUTE LUNG INJURY (TRALI) = LEUKO-AGGLUTINATION REACTION:
. Acute Shortness of breath from antibodies in the donor blood against the recipient WBCs.
. Ex -> 20 mins after a pt. receives a blood transfusion, the pt becomes short of breath.
. Transient infiltrates on CXR.
. All symptoms resolve spontaneously.
. 3 . IgA DEFECIENCY:
. presents with anaphylaxis !
. In the future, use blood donations from an IgA defecient donor or washed RBCs.
. Ex -> As soon as the pt. received transfus., he becomes SOB, hypotensive & tachycardic.
. NORMAL LDH & BILIRUBIN.
. 4 . MINOR BLOOD GROUP INCOMPATIBILITY:
. To kell, Duffy, Lewis or Kidd antigens or Rh incompatibility !
. Delayed jaundice.
. No specific therapy.
. Ex -> A few days after transfusion, the pt becomes jaundiced.
. The hematocrit doesn't rise with transfusion & he is generally without symptoms.
. 5 . FEBRILE NON-HEMOLYTIC REACTION:
. Small rise in temperature.
. No ttt required.
. Reaction against donor WBCs antigens.
. prevented by using filtered blood transfusions in the future to remove WBCs antigens.
. Ex -> A few hours after transfusion, the pt becomes febrile with rise 1 degree in temp.
. No evidence of hemolysis.
((RHINITIS))
{A} ALLERGIC RHINITIS:
. Watery rhinorrhea & sneezing with more prominent eye symptoms.
. Early age of onset.
. Identifiable trigger (animals - environmental exposure).
. Usually seasonal symptoms but can be persistent throughout year.
. Nasal mucosa can be normal, pale blue or pale on exam.
. Associated with allergic disorders e.g. eczema & asthma.
. Tx -> Allergen avoidance.
. Tx -> Topical intra-nasal glucocorticoids.
{B} NON-ALLERGIC RHINITIS = VASOMOTOR RHINITIS:
. Nasal congestion - Rhinorrhea - Postnasal discharge (postnasal drip = dry cough).
. Late age of onset > 20 ys.
. Can't identify clear trigger !
. Symptoms throughout the year but sometimes worse with seasons change.
. Nasal mucosa may be normal or erythematous.
. Less commonly associated with allergic disorders e.g. asthma or eczema.
. Routine allergy testing isn't necessary prior to initiating empiric ttt.
. May respond to 1st generation oral H1 antihistaminics (Chloramphenicol),
. Never ever responds to antihistaminics without anticholinergic properties (Loratidine)!
. Tx -> TOPICAL INTRANASAL GLUCOCORTICOIDS.
((The 3 most common causes of CHRONIC COUGH (> 8 weeks)))
. UPPER AIRWAY COUGH $YNDROME (Post-nasal drip).
. BRONCHIAL ASTHMA.
. GERD.
((UPPER AIRWAY COUGH $YNDROME = POST-NASAL DRIP))
. NON-smoker.
. Caused by rhino-sinusitis conditions.
. Dry cough is most likely due to post-nasal drip associated with allergic rhinitis.
. Dx -> Confirmed by improvement of the nasal discharge & cough with H1 Anti-histaminics.
. Chlorpheniramine is an H1 receptor blocker that decreases the allergic response.
. Decrease in NASAL SECRETIONS is most likely to significally improve symptoms. .
((ALLERGIC REACTIONS))
{1} . ANAPHYLAXIS = ANAPHYLACTIC SHOCK:
. Type 1 hypersensitivity reaction.
. Pts usually have prior exposure to the offending substance.
. Pts have preformed Ig E -> Histamine mediated peripheral vasodilatation.
. Bee stings - food & medications are the most common allergens.
. Acute onset of hypotension & tachycardia.
. Dangerous allergic reaction may progress to respiratory failure & circulatory collapse.
. Allergen exposure -> Sudden onset of symptoms in more than one system,
. Cutaneous (hives - flushing - pruritis).
. GIT ( Lip / tongue swelling - vomiting).
. Respiratory (Dyspnea - wheezing - stridor - hypoxia).
. Cardiovascular (Hypotension).
. It is a medical emergency.
. Tx -> INTRA-MUSCULAR EPINEPHRINE into the THIGH.
{2} . ANGIO-EDEMA:
. H/O of ICU pt on ACEIs e.g ENALAPRIL.
. Edema in the face, mouth, lips.
. Absence of pruritis & urticaria.**IMP**
. Laryngeal edema may occur causing airway obstruction.
. occurs due to BRADYKININ release.
. it may occur at any time not just at the start of drug intake.
. Dx----> Low levels of C2 & C4.
. Tx----> STOP ACEIs + FRESH FROZEN PLASMA + Secure the airway.

. HERIDITARY angioedema:
. C1 esterase inhibitor defeciency.
. usually follows an infection, dental procedure or minor trauma.
. N.B. The most common cause of acquired isolated angioedema is ACE inhibitors use.
. N.B. C1q is NORMAL in hereditary angioedema.
. N.B. C1q is DEPRESSED in acquired angioedema.
. C4 levels are depressed in all forms !
{3} . URTICARIA:
. Sudden swellings of the superficial layers of the skin.
. Can be caused by insects or medications.
. May be caused by pressure, cold or vibration !
. Tx -> ANTI-HISTAMINICs (Diphenhydramine & koratidine).
((GRAFT VERSUS HOST DISEASE (GVHD)))
. in pts with bone marrow transplantation.
. due to activation of the DONOR "T" lymphocytes.
. Skin ---> Maculopapular rash.
. Intestine ---> Bloody diarrhea.
. Liver ---> Abnormal LFTs & jaundice.
((WISKOTT - ALDRICH $YNDROME))
. IMMUNODEFECIENCY + THROMBOCYTOPENIA + ECZEMA.
. MARKED DECREASED T-LYMPHOCYTES.
. BM TRANSPLANTATION is the ONLY curative ttt.

PRIMARY IMMUNO-DEFECIENCY DISORDERS:
{1} COMMON VARIABLE IMMUNODEFECIENCY (CVID):
. ADULT with recurrent sino-pulmonary infections.
. NORMAL NUMBER OF "B" cells but don't make effective amounts of immunoglobulins.
. DECREASE in ALL subtypes of immunoglobulins (IgG, IgM & IgA).
. Frequent episodes of bronchitis, pneumonia, sinusitis & otitis media.
. CVID increases the risk of lymphoma.
. Dx -> Decreased immunoglobulins level & -- response to Ag stimulation of B-cells.
. Tx -> Antibiotics for infections.
. Tx -> Chronic maintenance with regular infusions of I.V. immunoglobulins.
. The clue to CVID is DECREASE in the OUTPUT of B-LYMPHOCYTES with,
. NORMAL NUMBER of B-cells & NORMAL amount of LYMPHOID TISSUE (LNs, adenoids & tonsils).
{2} X-LINKED (BRUTON) A-GAMMA-GLOBULINEMIA:
. MALE CHILDREN with recurrent sino-pulmonary infections.
. DIMINISHED B-cells & LYMPHOID TISSUES.
. ABSENCE of tonsils, adenoids & lymph nodes & spleen.
. NORMAL T-cells.
. Tx -> Antibiotics for infections.
. Tx -> Chronic maintenance with regular infusions of I.V. immunoglobulins. {3} SEVERE COMBINED IMMUNODEFECIENCY:
. Combined = Deficiency in BOTH B & T cells.
. -- B-cells -> -- immunoglobulin production -> Recurrent sinopulmonary infections at 6ms
. -- T-cells -> AIDS related infections e.g. PCP, varicella & candida.
. Treat the infections as they rise.
. BM transplantation is curative.
{4} Ig"A" DEFECIENCY:
. Recurrent sinopulmonary infections + ATOPIC DISEASE + ANAPHYLAXIS to blood transfusions
. Anaphylaxis from blood transfusions from pts with "NORMAL" levels of IgA !
. Treat infections as they arise.
. ONLY use blood that is from Ig-A DEFECIENT donors or that has been WASHED !
. IVIG will NOT work as the amount of IgA in the product is too small to be therapeutic !
. The trace amounts of IgA in IVIG may provoke anaphylaxis !
{5} HYPER Ig"E" $YNDROME:
. Recurrent SKIN infections with STAPHYLOCOCCI.
. Treat infections as they arise.
. Consider prophylactic antibiotics e.g Dicloxacillin & cephalexin.
{6} WISKOTT - ALDRICH $YNDROME:
. IMMUNODEFECIENCY + THROMBOCYTOPENIA + ECZEMA.
. MARKED DECREASED T-LYMPHOCYTES.
. BM TRANSPLANTATION is the ONLY curative ttt. {7} CHRONIC GRANULOMATOUS DISEASE (CGD):
. Genetic disease results in extensive inflammatory reactions.
. Lymph nodes with purulent material leaking out !
. Aphthous ulcers & inflammation of the nares.
. Obstructive granulomas in the GIT or UT.
. Infections with odd combinations (Staphylococci, Bulkhorderia, Nocardia & Aspergillus).
. Dx -> ABNORMAL TETRAZOLIUM TEST !
. -- in respiratory burst that produces hydrogen peroxide.
. -- in NADPH oxidase that generates superoxide.
=============================================================================================
PREVENTIVE MEDICINE
AAA
The USPSTF recommends one-time screening for abdominal aortic aneurysm (AAA) with ultrasonography in men ages 65 to 75 years who have ever smoked.
ALCOHOL
The USPSTF recommends that clinicians screen adults aged 18 years or older for alcohol misuse and provide persons engaged in risky or hazardous drinking with brief behavioral counseling interventions to reduce alcohol misuse
ASPIRIN
The USPSTF recommends the use of aspirin for men age 45 to 79 years
The USPSTF recommends the use of aspirin for women age 55 to 79 years
The USPSTF recommends against the routine use of aspirin and nonsteroidal anit-inflammatory drugs (NSAIDS) to prevent colorectal cancer in individuals at average risk for colorectal cancer.
ASYMPTOMATIC BACTERIURIA
The USPSTF recommends screening for asymptomatic bacteriuria with urine culture for pregnant women at 12 to 16 weeks' gestation or at their first prenatal visit, if later.
BLOOD PRESSURE
The U.S. Preventive Services Task Force (USPSTF) recommends screening for high blood pressure in adults 18 and over.
BREAST CANCER
The USPSTF recommends biennial screening mammography for women 50-74 years.
The USPSTF recommends against teaching breast self-examination (BSE).
SYPHILIS
The USPSTF recommends that clinicians screen all pregnan

[ArchivalUser]

“high yields”
 know the different types of shock- hypovolemic, septic, cardiogenic (CO, MAP,
SVR)
 metabolic acidosis leads to hyperkalemia
 diabetes mellitus and rhizopus/mucormycosis infections.
 optic neuritis is associated with multiple sclerosis
 hemolytic uremic syndrome after gastrointestinal illness w/ 1) acute renal failure
2) microangiopathic hemolytic anemia 3) thrombocytopenia
 hypertension is most important risk factor for strokes
 ACEi and diabetes mellitus. ACEis decrease GFR and FF (dilates efferent arteriole)
 theophylline toxicity manifests as CNS (headache, insomnia),
gastrointestinal (nausea, vomiting), cardiac (arrhythmias)
 renal transplant dysfunction can be caused by a variety of factors. acute
rejection is best treated w/ steroids.
 thiazide diuretics cause hyperglycemia, increased LDL cholesterol,
increased triglycerides. hyperuricemia (gout), hypercalcemia (protects
against calcium stones)
 beckwith-wiedemann syndrome has macrosomia, macroglossia,
visceromegaly, omphalocele, hypogylcemia, and hyperinsulinemia. Babies with
thyroid disorder will have umbilical herniation.
 lifestyle modifications to decrease BP: lose weight > fruits and vegs > decrease
sodium > exercise > alcohol intake
 hyperosmolar nonketosis (HONK) occurs in type 2 diabetes mellitus. have severe
hyperglycemia resulting in dehydration.
 SIRS criteria 2 of the following: 1) temp > 101.3 or < 95 2) pulse > 90 3) resp >
20 4) WBC > 12k or
water retention and elevation of total body volume
 pericardial effusions appear as enlarged "water bottle" shaped cardiac
silhouette. pericardial effusion will have a non-palpable point of maximal
impulse, diminished heart sounds
 pericardial effusion and cardiac tamponade have: hypotension, distended
neck veins (high int. jugular venous pressure), and muffled heart sounds. will also
have positive hepatojugular reflex and pulsus paradoxus. fluid
accumulation in the pericardial cavity that increases the intrapericardial pressure
above the diastolic ventricular pressure. restricts venous return to the heart.
decreases diastolic filling and lowers preload.
 infective endocarditis can present with systemic arterial emboli (cns, renal,
splenic), glomerulonephritis, roth spots, osler’s nodes, janeway lesions, mycotic
aneurysms
 dihydropyridine (-dipine) calcium channel blockers like amlodipine can
cause peripheral edema.
 strongest influence on long-term prognosis for an ST-elevation MI is the duration
of time that passes before coronary blood flow is restored via PTCA or fibrinolysis.
 for BP control weight loss is most important intervention. weight loss >
physical activity > salt restriction > alcohol
 mitral regurgitation is a holosystolic murmur radiating to axilla. will have
soft s1 because improper closure of the mitral valve.
 aortic regurgitation has a wide pulse pressure (systolic – diastolic) which
patients experience as a “pounding” heartbeat. lying flat brings heart closer to
chest wall and patients are more aware of the forceful heartbeat.
 constrictive pericarditis caused by pericardial fibrosis and obliteration of
pericardial space. presents like chf (fatigue, dyspnea on exertion, muscle wasting,
elevated jvp, ascites, positive kussmaul’s sign - increase jvp on
inspiration), pedal edema. in developing countries can be caused by
tuberculosis.
 give nitroglycerine for cardiogenic pulmonary edema. will decrease
preload and relieve dyspnea and tachycardia. cardiogenic pulmonary edema will
have bibasilar rales and wheezing as well.
 digoxin and furosemide/loop diuretics reduce congestive heart failure
symptoms but do not improve survival.
 patients with a history of rheumatic fever have an increased risk of recurrent
episodes and progression of rheumatic heart disease with repeated infection by
group A streptococcus pharyngitis. need penicillin prophylaxis.
 class IC anti-arrhythmics (flecainide/propafenone) block sodium channels.
they elongate period of depolarization, and prolong the action potential. slower
conduction through the AV node and his-purkinje system. class IC meds have the
slowest binding and dissociation from the sodium channel. flecainide is a
IC that demonstrates “use-dependence” where the HR increases flecainide’s
effect on the sodium channels. Flecainide is stronger at faster heart rates. there is
less time between APs for the medication to dissociate from it’s receptor. so the
QRS complex will prolong as the HR increases.
 aortic stenosis needs echocardiogram to confirm diagnosis. if symptomatic
then treat with valve replacement.
 long QT syndrome can present as syncopal episodes, hearing loss, and a
family history of sudden cardiac death. treat with beta blockers
 mitral regurgitation can cause a holosystolic murmur that radiates to the
axilla. Mitral valve prolapse is the most common cause of mitral regurgitation.
mitral regurgitation can lead to left atrial dilation and atrial fibrillation.
 digoxin toxicity side effects are gastrointestinal (anorexia, nausea, vomiting).
verapamil increases digoxin concentrations and predisposes to toxicity.
 mitral stenosis has a loud s1 and a mid-diastolic rumble. can cause atrial
fibrillation because of left atrial dilation
 causes of pulsus paradoxus include cardiac tamponade, tension
pneumothorax, and severe asthma. > 10 mmHg drop in systolic blood
pressure on inspiration.
 cor pulmonale has hypotension, jvd, distant heart sounds, and pulsus
paradoxus. elevated jvp, hepatomegaly, ascites, lower extremity edema without
evidence of pulmonary congestion is suggestive of isolated right sided heart
failure, cor pulmonale. most common cause is COPD.
 in a patient with an MI who develops a clot, do echocardiogram to rule out
thrombus in left ventricle.
 in ventricular fibrillation and pulseless ventricular tachycardia, defibrillation is
the treatment. Ventricular fibrillation is recognized on EKG by fibrillatory
waves and absence of regular qrs complexes. time to defib is correlated with
survival.
 a CXR should be obtained in all patients who undergo central venous
catheterization to confirm proper placement of the catheter tip before
administering drugs or other agents through the catheter.
 acute MI presents with substernal chest pain with radiation to neck, diaphoresis,
shortness of breath. a new 4th heart sound is a classic finding of myocardial
infarction. ischemic damage may lead to diastolic dysfunction and a stiffened
left ventricle, resulting in an atrial gallop (4th heart sound)
 abdominal ultrasound is the study of choice for diagnosis and follow-up of
abdominal aortic aneurysms. nearly 100% sensitive and specific for this
condition
 mitral stenosis classically presents during pregnancy. most often due to
rheumatic fever and occurs much more often in countries with limited access to
antibiotics. There is an increase in plasma volume with pregnancy.
 an exercise stress test without imaging is the most reasonable first step if
baseline resting EKG is normal in a patient complaining of exertional cardiac pain.
 if patients are hemodynamically unstable and have sustained monomorphic
ventricular tachycardia (SMVT) then electrically cardiovert, but if they are
stable and asymptomatic you can give anti-arrhythmics (amiodarone). SMVT is a
wide complex tachycardia.
 in patients who present with abdominal pain and have risk factors for
myocardial infarction, rule out myocardial infarction before further
gastrointestinal workup
 coarctation of the aorta presents with severe symptomatic hypertension
(headaches, epistaxis, and evidence of left ventricular hypertrophy). EKG will
show increased voltage of QRS complexes and ST and T wave changes in
left precordial leads. all patients (especially young) with systemic hypertension
should be evaluated for coarctation with simultaneous palpation of brachial and
femoral pulses to assess for brachial-femoral delay. also have supine bilateral
arm (brachial) and prone right and/or left leg (popliteal) blood pressures
measured to assess for differential pressures. coarctation may be congenital or
acquired (takayasu)
 cardiac tamponade produces a decrease in CO because the pressure exerted on
the heart by the pericardial fluid is greater than the venous pressure that fills the
right atrium during diastole. pulsus paradoxus is a feature of tamponade and is
defined as a large decrease in the systolic blood pressure on inspiration.
demonstrated by loss of a palpable radial pulse during inspiration.
 Superior vena cava syndrome is a potential complication of lung malignancy, and
is manifested by headache, facial swelling, and jugular venous
engorgement without peripheral edema. headaches worse when leaning
forward due to decreased gravitational effects on the blood column. jvd is
present, but there is no peripheral edema to suggest cardiac failure. the primary
treatment is radiation therapy as a palliative measure.
 EKG with wide-complex tachycardia with monomorphic ventricular
tachycardia in a stable patient is treated with amiodarone.
 peripheral vascular disease should be suspected in a patient with risk factors
for atherosclerosis who has an extremity with shiny, thin, hairless skin,
particularly if a non-healing ulcer is present. use ankle-brachial index to assess
pvd.
 septic shock has impaired circulation resulting in insufficient oxygen delivery to
the peripheral tissues and subsequent anaerobic metabolism. leads to an
increase in the production of lactic acid producing metabolic acidosis
 myocarditis can lead to the development of dilated cardiomyopathy.
bibasilar crackles, pitting edema, and displacement of the point of
maximal impulse.
 patients with mitral valve prolapse have a slightly higher risk of developing
infective endocarditis after certain invasive procedures. 2007 AHA guidelines for
the prevention of infective endocarditis do not recommend anti-microbial
prophylaxis for patients with mitral valve prolapse including those with
regurgitation. if you have prosthetic heart valves, previous history of
infective endocarditis, or unrepaired congenital heart disease you get
prophylaxis.
 atrial fibrillation has irregularly irregular QRS complex, absent P waves.
treatment is rate control or rythm control and anti-coagulation. to treat rate use
beta-blocker or verapamil/diliazem.
 Atrial septal defect has wide, fixed splitting of s2. patients with moderate to
severe left to right shunts may have a systolic murmur best heard at the upper
left sternal border from increased blood flow across pulmonic valve.
 septic shock should be suspected in patients with hemodynamic instability and
evidence of an infection. initial treatment is iv fluids followed by vasopressors
(dopamine or norepinephrine) if they do not respond to fluids.
 as mitral stenosis becomes more severe, the transvalvular gradient increases
and causes the murmur to be heard earlier in diastole at the apex. early
diastolic murmur at left lower sternal border is heard in patients with aortic
regurgitation.
 systolic murmur that increases with decreased preload (standing) is mitral
valve prolapse or hypertrophic obstructive cardiomyopathy. in mvp there
is a mid-systolic click and a late systolic murmur best heard at apex. in hocm the
murmur increases when standing because of less venous return and the left
ventricular outflow tract obstruction worsens. more common in young
african americans.
 Hypotension is caused by a decreased left ventricular preload in a
hemothorax. (similar mechanism as tension pneumo). hemothorax will have lack
of breath sounds, and dullness to percussion on the ipsilateral side as the
hemothorax due to accumulation of fluid in the pleural space. hemothorax is a
potential complication of thoracentesis and should be suspected in patients
who rapidly reaccumulate a pleural effusion, difficulty breathing, and
hemodynamic instability shortly after a thoracentesis
 venodilation decreases the pain associated with acute myocardial infarction by
reducing preload, leading to a reduction in myocardial oxygen demand.
 aortic regurgitation is a diastolic decrescendo murmur over left sternal
border. aortic regurgitation commonly due to aortic root dilation or a bicuspid
valve.
 flattening of P wave, prolonged PR and QRS are consistent with
hyperkalemia. give calcium gluconate to stabilize cardiac cell membrane.
hypokalemia has u waves, flat and broad T waves.
 ruptured abdominal aortic aneurysm is an important cause of abdominal and
referred lower abdominal pain. patients also have atherosclerosis of other vessels
such as coronary or carotid arteries.
 cyanosis in highly vascularized tissues like lips and mucous membranes is
consistent witth central cyanosis. peripheral cyanosis usually only involves the
distal extremities. central cyanosis is caused by low arterial oxygen
saturation, peripheral cyanosis is due to increased oxygen extraction (proximal
tissues take all the oxygen, and distal extremities get none??) secondary to
sluggish blood flow. in peripheral cyanosis the extremities are cool and
clammy.
 lipemic serum (milky and opalescent) along with palmar xanthomas is
consistent with severe hypertriglyceridemia. treat with fibric acid derivatives
like fenofibrate.
 arrhythmia has sudden-onset syncope without a prodrome. sotalol used to
maintain sinus rythm (in patients with atrial fibrillation) has a side effect of
prolongation of the QT interval which predisposes to torsades de pointes.
hypokalemia and hypomagnesemia (from diarrhea) are predisposing
factors. QT interval prolongation and PR interval prolongation. treat with
magnesium sulfate (not anti-arrhythmics) initially.
 wolff-parkinson-white (wpw) synrome is characterized by an accessory pathway
between the atrium and ventricle resulting in preexcitation and increased risk for
tachyarrhythmias. the accessory pathway conducts antegrade (forward) from
atria to the ventricles faster than the conduction through the av node, which
allows part of the ventricle to depolarize early. shortened PR interval, slurred
initial portion of QRS (delta wave) and widened QRS complex.
 before exercise EKG withhold medications that are anti-ischemic and/or slow
the heart. beta-blockers should be withheld 12-24 hours before the test.
 most common cause of death in patients with acute myocardial infarction is
complex ventricular arrhythmia. acute ischemia creates a heterogeneity of
conduction in the myocardium. areas of partial block of conduction are
frequently formed that predispose the patient to reentrant arrhythmia.
Ventricular fibrillation is a typical example of reentrant arrhythmia.
 paroxysmal supraventricular tachycardia most commonly results from
accessory conduction pathways through the av node. vagal maneuvers and
medications that decrease conduction through the av node (adenosine)
often resolve the PSVT.
 pericarditis presents with pain that worsens with deep inspiration, improved
on leaning forward. EKG findings show diffuse ST elevation with the exception
of reciprocal depression in aVR where ST depression is seen. dressler’s
syndrome is pericarditis occuring weeks after a myocardial infarction. NSAIDs are
the mainstay of therapy for dressler’s syndrome.
 progressive decrease in baroreceptor sensitivity and defects in the
myocardial response to this reflex are the main reasons for increased
orthostatic hypotension in the elderly. (blood pressure drops, heart rate should
increase to compensate)
 screen patients who are 65 - 75 and who have smoked cigarettes before with
abdominal ultrasound for abdominal aortic aneurysm.
 athero-embolism results from dislodgement of cholesterol plaques from the aortic
root. “blue toe syndrome” in which emboli to the pedal circulation cause cyanotic
and painful toes with intact pulses is one common presentation of catheterinduced
atheroembolism. may be accompanied by livedo reticularis (purple
mottled skin), and elevation of creatinine resulting in atheroembolism of
renal circulation.
 all patients who have had a myocardial infarction should recieve secondary
prevention. the following medications have been shown to have a mortality
benefit when given as 2nd prevention: aspirin, beta-blocker, ACEi, lipid
lowering statin, clopidogrel/ticlopidine (if they are post percutaneous
coronary intervention).
 digoxin is a cardiac glycoside with adverse effects that include gastrointestinal
disturbances, vision changes, and arrhythmias. patients taking digoxin should
have routine monitoring of their digoxin level.
 peripheral vascular disease commonly caused by atherosclerosis. presents
with claudication, erectile dysfunction, and atypical leg pain or can be
asymptomatic. take the ankle-brachial index (abi) using doppler as the first step
to diagnose in high-risk of symptomatic patients. do exercise testing with preexercise
and post-exercise abi measurement to confirm diagnosis.
 fever, chills, LUQ pain, and splenic fluid collection suggests findings consistent
with infective endocarditis with septic emboli to the spleen. left sided
endocarditis can send septic emboli to regions rich in blood supply: brain,
kidneys, liver, spleen. right sided endocarditis tends to send septic pulmonary
emboli. will have elevated neutrophils.
 fever and a new murmur in a patient who may abuse iv drugs should raise
concern for endocarditis. staphylococci (incl. MRSA) is a more common cause of
endocarditis in ivda, therefore vancomycin is the initial empiric antibiotic
of choice.
 abdominal aortic aneurysm rupture presents with profound hypotension,
abdominal or back pain followed by syncope, and possible pulsatile mass on
examination. aaa can rupure into the peritoneum and create an aortocaval
fistula with the inferior vena cava leading to venous congestion in
retroperitoneal structures (e.g. bladder). the fragile and distended veins in the
bladder can rupture and cause gross hematuria.
 ascending aortic aneurysms are most often due to cystic medial necrosis or
connective tissue disorders. Descending/thoracic aortic aneurysms are
usually due to atherosclerosis.
 diastolic dysfunction is also called heart failure with preserved left
ventricular ejection fraction. systemic hypertension is the classical cause of
diastolic dysfunction. treatment is with diuretics and bp control.
 dilated cardiomyopathy can occur secondary to acute viral myocarditis
(coxsackie b, parvo b19, hhv6, adeno, entero). viral myocarditis causes dilated
cardiomyopathy via direct viral damage and as a result of humoral or cellular
immune responses to viral infections. diagnose via echocardogram which shows
dilated ventricles with diffuse hypokinesia resulting in a low ejection fraction.
 hepato-jugular reflex can be used to differentiate between heart and liver
disease-related causes of lower extremity edema. +hepato-jugular reflex
indicates that the venous pressure is elevated and suggests that heartdisease
related edema is present. hepato-jugular reflex is negative in patients
with liver disease related edema.
 cool dusky fingertips after vasopressors can be the result of
norepinephrine-induced vasospasm. norepinehrine has alpha-1 agonist
properties which cause vasoconstriction, which is good when trying to
increase the bp of hypotensive patients, however in patients with decreased
blood flow it can cause ischemia and necrosis of distal fingers/toes. can also
occur in intestines (mesenteric ischemia) or kidney (renal failure)
 native valve bacterial endocarditis due to S. viridans highly susceptible to
penicillin is well-treated with iv penicillin g or iv ceftriaxone. do not use oral
antibiotics for subacute bacterial endocarditis.
 symptomatic sinus bradycardia should be treated with iv atropine, followed
by trancutaneous pacing. if they are hemodynamically unstable the use of
epinephrine is appropriate. (do no confuse with adenosine for PSVT !!!!!)
 three most common causes of aortic stenosis are 1) senile calcific aortic
stenosis, 2) bicuspid aortic valve and 3) rheumatic heart disease. bicuspid
aortic valve is the cause of aortic stenosis in the majority of patients < 70 y/o.
systolic murmur in right upper sternal border with radiation to the carotids.
 aortic regurgitation causes an early diastolic murmur and can be associated
with a hyperdynamic pulse, including bounding or “water hammer”
peripheral puses.
 acute pericarditis is characterized by sharp pleuritic chest pain that is worse
in the supine position and improved by sitting up and learning forward. occurs in
the first several days after myocardial infarction. diffuse ST elevations,
especially with PR depressions are typical EKG findings.
 outflow obstruction in hypertrophic obstructive cardiomyopathy results from
both septal hypertrophy and systolic anterior motion (SAM) of the mitral
valve. hocm presents as crescendo-decrescendo murmur in the lower left
sternal border. increases during valsalva due to decreased preload and decreased
filling of left ventricle.
 EKG findings in acute pericarditis are diffuse ST elevation and depression
of PR segment (except in aVR). most common cause is viral infection. can
also be caused by uremia (patient with renal problems). treatment of uremic
pericarditis is dialysis. indications for hemodialysis are 1) refractory
hyperkalemia 2) volume overload or pulmonary edema not responding to
diuretics 3) refractory metabolic acidosis (ph < 7.2) 4) uremic pericarditis 5)
uremic encephalopathy or neuropathy 6) coagulopathy due to renal failure
 kussmaul’s sign (increased jvp on inspiration) is seen in: constrictive
pericarditis, cardiac tamponade, right heart failure. hypotension, jvd and
clear lung fields point to right ventricular infarction. treat with iv fluids and
avoidance of preload reducing medications (nitrates and diuretics), they are
preload dependent. right heart failure = liquids
 cardiac cath is typically done by cannulating the femoral artery to access the
cardiac vessels. a common complication is hematoma formation in soft
tissues of the upper thigh. if the arterial puncture was done above the
inguinal ligament, this hematoma can extend directly into the
retroperitoneal space and cause significant bleeding, with hypotension and
tachycardia. patients can also develop ipsilateral flank pain/back pain and
neurologic defects on the ipsilateral side. next step would be to obtain a CT
of the abdomen and pelvis without contrast to confirm.
 acute heart failure can cause pulmonary edema or “flash pulmonary edema”
secondary to anterior wall myocardial infarction. a diuretic such as furosemide is
the drug of choice in this setting. decreases the cardiac preload thereby
decreasing the pulmonary capillary pressure. also causes venodilation which
further decreases preload.
 clear lung fields, hypotension, and jugular venous distension in the setting of an
inferior wall mi are suggestive of a right ventricular infarct. fluid
resuscitation is the appropriate management, and nitrates should be
avoided because they decrease preload and will limit cardiac output.
 anterolateral myocardial infarction can cause papillary muscle ischemia
or rupture, which can cause mitral regurgitation. will have bibasilar crackles,
orthopnea. measurement of pulmonary capillary wedge pressure (PWCP/left atrial
pressure) with a swan-ganz catheter will reveal increased pressure in the left
atrium
 premature ventricular complexes (PVCs) are common in post-myocardial
infarction patients and can be recognized by their widened QRS > 120
msec, bizzare morphology, and compensatory pause. no treatment unless
symptomatic.
 amyloidosis can result in a restrictive cardiomyopathy with thickened
ventricular walls and preserved ventricular dimensions as well as liver
(clotting, bruising) and kidneys (proteinuria)
 calcium gluconate is given for hyperkalemia to protect the heart. on EKG
hyperkalemia will have peaked T waves, and prolongation of PR and QRS
intervals eventually leading to a sine wave. sodium bicarb is used in TCA and
aspirin overdose. magnesium sulfate is used for torsades de pointes. a
polymorphic ventricular tachycardia associated with a prolonged QT
interval. it commonly occurs in patients with long QT syndrome as well as
patients with a history of alcoholism and recent intiation of fluconazole and
moxifloxacin.
 myocarditis presents as a flu-like illness with fever, anorexia, lethargy, irritability
in children. followed by respiratory distress from acute heart failure. CXR will
show cardiomegaly and pulmonary edema. EKG shows low voltage QRS and
sinus tachycardia. echocardiogram shows global hypokinesis, left
ventricular hypertrophy, left ventricular dysfunction, and pericardial
effusion. gold standard is myocardial biopsy.
 aortic stenosis can cause anginal chest pain because the left ventricle will
hypertrophy requiring additional oxygen. increased myocardial oxygen
demand
 myocarditis presents like congestive heart failure with cardiomegaly,
paroxysmal nocturnal dyspnea, dyspnea on exertion, peripheral edema,
hepatomegaly, bilateral pleural effusions, and a third heart sound. viral
myocarditis is often due to coxsackie b virus.
dermatology
 senile purpura is characterized by ecchymoses that occur on elderly patients
extensor surfaces due to perivascular connective tissue atrophy. renal
failure can also cause platelet dysfunction, creatinine would be elevated.
 basal cell carcinoma in sun exposure. nodule with pearly rolled borders and
telangiectasia
 actinic keratosis described as erythematous papules with a central scale.
"sandpaper like" texture. sun exposed areas
 stevens johnson = erythema multiforme major. target shaped muco-cutaneous
lesions and systemic signs of toxicity. type 3 hypersensitivity
 eschar formation can compromise blood flow and lymphatic circulation. decreased
pulses and edema. do escharotomy.
 sq. cell carcinoma with chronic wounds.
 rosacea in middle-aged patietns with telangiectasias over cheeks, nose, and
chin. flushing made worse by hot/cold drinks, sun, emotion. has papules and
pustules. tx is metronidazole
 porphyria cutanea tarda has painless blisters, photosensitivity, increased
skin fragility on dorsum of the hands, hypertrichosis. associated with hep c
infection (think liver stuff)
 tinea corporis has ring-shaped scaly patches with a central clearing and
scaly borders. treatment is terbinafine.
 normal skin @ birth with progression to dry, scaly skin with horny plates over
extensor surfaces is icythosis vulgaris. worsens in winter. looks like lizardy
skin
 allergic contact dermatitis has vesicles at the site of exposure. can become
secondarily infected and have pus filled vesicles.
 for SCC do a punch biopsy to confirm dx
 vitiligo is due to autoimmune destruction of melanocytes
 seborrheic keratosis is a benign growth that occurs in many places on the
body, but favors face/trunk. the lesions have a waxy, stuck on, warty and well
circumscribed appearance. actinic keratosis is a pre-malignant lesion that is
dry, scaly, flat papule with erythematous base.
 bullous pemphigoid is autoimmune blistering disorder marked by tense bullae,
urticarial plaques. igg and c3 along basement membrane zone.
 the most common drugs in the treatment of acne to produce phototoxic drug
reactions are the tetracyclines, namely doxycycline. sunburn reactions with
erythema, edema, and vesicles over sun-exposed areas.
 squamous cell carcinoma is the 2nd most common form of non-melanoma skin
cancer after basal cell carcinoma. exposure to sunlight is the most important
factor in the development of scc.
 best way to prevent malignant melanoma is wearing protective clothing. sun
screen protects against non-melanoma skin cancer like sq. cell carcinoma
 for basal cell carcinoma do mohs surgery, wherein microscopic shaving is
done such that 1-2mm of clear margins are excised. this technique has the
highest cure rate for basal cell cancer. but is indicated only in patients with highrisk
features or in those with lesions in functionally critical areas (perioral, nose,
lips, ears)
 pemphigus vulgaris is a mucocutaneous blistering disease that is characterized
by flaccid bullae and intercellular igg deposits in the epidermis. autoantibodies
are formed against desmoglein, an adhesion molecule. bullous pemphigoid
rarely has oral lesions. (not in mucous membranes)
 dermatitis herpetiformis is associated with gluten-sensitive enteropathy
(celiac disease). dapsone is an effective treatment.
 mild acne (non-inflammatory comedones) are treated with topical retinoids
first. topical antibiotics are added with mild-to-moderate inflammatory
acne. use oral isoretinoin for patients with nodulocystic and scarring acne.
 seborrheic dermatitis is a common inflammatory disease that affects areas
with sebaceous glands, such as the scalp (dandruff) face (eyebrows
nasolabial folds and external ear canal/posterior ear), chest and
intertriginous areas. seborrheic dermatitis occurs in all ages but is found in
increased frequency in patients with parkinsons and hiv. pruritic erythematous
plaques with fine, loose, yellow, and greasy looking scales. acne rosacea is
a rosy hue with telangiectasia over the cheeks, nose and chin. flushing of
these areas is typically precipitated by hot drinks, heat, emotion, and other
causes of rapid body temp changes.
 atopic dermatitis (eczema) in infancy affects face, scalp, and extensor
surfaces of the extremities. lesions usually begin with pruritis alone, and
evolve to erythematous excoriated papules and plaques that may weep and
become secondarily impetiginized. atopic dermatitis is the result of
decreased skin barrier function due to improper synthesis of components of
the epidermal cornified cell envelope. allergens can readily access deeper levels
of the epidermis where they may generate the immune resopnse. the diaper
region is typically spared.
 excisional biopsy with narrow margins is the preferred study for the
diagnosis of melanoma. if the depth of the lesion is 1 mm in depth should have a sentinel lymph node study. do not do
excision with wide margins (like 1 cm) until the diagnosis of melanoma
is made.
 toxic epidermal necrolysis is a severe mucocutaneous exfoliative disease.
erythematous morbiliform eruption that rapidly evolves into exfoliation of
the skin. in steven johnson syndrome up to 10% of the body surface area is
involved, in TEN > 30% of the body surface is involved.
 molluscum contagiosum caused by poxvirus. dome shaped lesions with
central umbilication.
 acne from steroids has no comedones and monomorphous pink papules.
adolescent acne has both open and closed comedones.
electrolytes
 chronic alcoholism -> pancreatitis -> malabsorption. low vitamin D means will
have low phosphorous and low calcium
 malignancy is the most common cause of hypercalcemia in admitted patients.
osteolytic mets, secretion of pth-rp, increased vit d, and IL-6
 hypocalcemia causes increased deep tendon reflexes. can occur after
multiple transfusions. hypermagnesemia has decreased deep tendon
reflexes.
 for hyperkalemia 1) stabilize membrane with calcium gluconate 2)
insulin/glucose and 3) remove from body (kayexalate)
 for a patient with severe hypovolemic hypernatremia give 0.9% saline
(isotonic saline). patients with less severe hypovolemic hypernatremia are
treated with 5% dextrose in 0.45% saline
 for calcium check the corrected calcium using ( 0.8 x 4.0 - measured alb) +
measured calc. do corrected calcium to see if hypoalbuminemia is causing
hypocalcemia. 0.8 x (4.0 – serum alb) + calcium. if the calcium falls in normal
range it’s due to hypoalbuminemia
 primary hyperparathyroidism is the most common cause of hypercalcemia in
ambulatory patients. in most cases it’s a solitary parathyroid adenoma.
 in patient with acute hyponatremia correct sodium concentration with 3%
saline (hypertonic).
 albuterol given for acute asthma attacks may cause hypokalemia, tremors,
palpitations and headache. beta-agonist --> hypokalemia
 hypokalemia has u waves and flat and broad t-waves on ecg, and premature
ventricular beats.
 meds causing hyperkalemia: digoxin, succinylcholine, tmp-smx, aceis,
nsaids, potassium-sparing diuretics like spironolactone and amiloride.
 treat hypercalcemia with iv saline hydration (normal saline 0.9%) followed
with loop diuretics (furosemide)
 bartter syndrome (can’t absorb NaCl) presents like renin secreting tumor with
very high >40 urine chloride, elevated plasma renin/aldosterone, low serum
k, high serum bicarbonate, but in bartter / gitelman syndrome the serum
Na is normal, in a renin secreting tumor serum sodium is elevated. renin
secreting tumors will also cause hypertension. bartter syndrome has defective
Na and chloride reabsorption in the thick ascending limb of the loop of
henle so you get hypovolemia --> raas. gitelman syndrome is like bartter
but defect in distal conv. tubule. basically bartter = normal serum na + lots
of raas
 asymptomatic hypercalcemia is the most common presentation for primary
hyperparathyroidism. 24 hour urinary calcium can help distinguish primary
hyperpth (>200 mg) from familial hypocalciuric hypercalcemia (200) and a high urine sodium
concentration ( urine na >30meq/l)
 to determine cause of hyponatremia calculate serum osmolality = (2 * na) + (bun
/ 2.8) + (glucose/18) if they are hypotonic and hyponatremic then look at volume
status: hypovolemic, euvolemic, or hypervolemic. hypovolemic hypotonic
hyponatremia can be due to renal or exrarenal losses of sodium and water.
extrarenal losses have a urine na < 10, (renal losses will have urine Na > 20) and
can be secondary to diarrhea and vomiting
 volume resuscitation with normal saline will correct contraction alkalosis.
hypokalemia should be treated as well.
 in patients with malignancy, hypercalcemia is due to the increased resorption
of bone and release of calcium from bone. the pathology involves osteolytic
mets with local release of cytokines and tumor secretion of pth-rp.
bisphoshonates are the drug of choice for mild to moderate hypercalcemia due
to malignancy. iv fluids and furosemide are used in the treatment of
hypercalcemic crisis.
 isotonic solutions such as normal saline (0.9%) are the fluid of choice for initial
resuscitation in severe hypovolemic hypernatremia.
 chronic renal failure can increase pth leading to 2nd hyperparathyroidism. seen
with moderate to severe renal insufficiency. serum calcium levels are normal to
low in patients with 2nd hyperpth because the cause of elevated pth is
hypocalcemia. primary hyperpth will have an elevation of pth and calcium
levels along with a history of renal stones and osteoporosis.
 vigorous hydration with iv normal saline is first step in managing severe
symptomatic hypercalcemia
 renal failure causes hypocalcemia. immobilization of an individual with a
high bone turnover results in increased osteoclastic activation that can
lead to hypercalcemia. bisphosphonate therapy in patients who are
immobilized is helpful in reducing hypercalcemia and preventing
osteopenia.
 vomiting causes metabolic alkalosis (losing volume and losing H+) with
hypochloremia and hypokalemia. volume contraction causes secondary
hyperaldosteronism causing hypokalemia. it will have low urine chloride metabolic alkalosis
emergency
 for ethylene glycol poisoning use fomepizole. will have calcium oxalate
stones in the kidneys. flank pain, hematuria, oliguria, acute renal failure, anion
gap metabolic acidosis.
 iron poisoning has a corrosive effect on the gi mucosa. ab. pain, nausea,
vomiting, diarrhea and hematemesis. hypotension and venodilation lead to
hypoperfusion and leads to metabolic acidosis. iron is radio-opaque so it can be
seen in stomach on abdominal xr. To diagnose measure serum iron levels, to
treat use iv deferoxamine
 when patient ingests acetaminophen, before giving n-acetylcysteine make
sure serum level is toxic (check at 4 hours). can give n-aceylcysteine within 8
hours of ingestion. give activated charcoal is good within 4 hours.
 when a patient ingests lye (sodium hydroxide) which is a strongly alkaline
solution, must do upper gi endoscopy to assess extent of esophageal injury
and determine if any further management is needed. if perforation is
suspected do a gastrografin study.
 sodium bicarbonate is used to treat TCA poisoning. tca overdose causes
hyperthermia, seizures, hypotension, and anti-cholinergic effects: dilated
pupils, flushed and dry skin, intestinal ileus and QRS prolongation. blind
as bat, dry as bone, hot as hare, mad as hatter, red as beet.
 diphenhydramine overdose presents with anti-cholinergic symptoms,
drowsiness, and confusion. diphenhydramine is an anti-histamine but can give
anti-cholinergic effects as well. treatment involves giving administration of
physostigmine, a cholinesterase inhibitor which reverses it’s effecs.
 for frostbite injuries, best treatment is rapid re-warming with warm water.
after warming, re-evaluate the extremity. amount of debridement is always less
after re-warming.
 methanol intoxication can cause vision loss and coma. physical exam will
show optic disc hyperemia, lab studies will show anion gap metabolic acidosis.
increased osmolar gap is often seen as well.
 in heat stroke the temperature is usually > 105F/40.5C. heat stroke results from
an insufficient evaporative cooling mechanism. treatment involves evaporative
cooling to reverse hyperthermia.
 opioid withdrawal presents with symptoms of nausea, vomiting, abdominal
pain, diarrhea, arthralgias and myalgias. signs of opioid withdrawal on exam can
include increased bowel sounds, mydriasis and piloerection. treat with
methadone. C. difficile infections generally do not begin until 5-10 days after
antibiotic treatment is initiated.
 bradycardia, av block, hypotension and diffuse wheezing indicate betablocker
overdose. most common presentation of beta blocker toxicity is
bradycardia and hypotension, which can lead to cardiogenic shock.
bronchospasm (diffuse wheezing) neurological effects (delirium and seizures) and
hypoglycemia. first give iv fluids and atropine, then give glucagon to increase
cAMP and higher levels of intracellular calcium to augment cardiac contractility.
 cocaine related cardiac ischemia is treated with benzodiazepines, nitrates,
and aspirin. beta-blockers are contraindicated.
 iron tablet intoxication appears as abdominal pain and hematemesis,
hypovolemic shock and metabolic acidosis. will appear radioopaque (can see)
on xr. give deferoxamine.
 sodium bicarbonate narrows QRS complex preventing development of
arrhythmia in patients with TCA toxicity by alleviating the cardio-depressant
action on sodium channels.
 caustic poisoning does not cause alterations in consciousness. presents with
dysphagia, severe pain, heavy salivation and mouth burns. the damage is the
result of necrosis of the tissue that lines the gastrointestinal tract. in severe
cases perforation of the stomach or esophagus can occur, causing peritonitis or
mediastinitis.
 give atropine to reverse organophosphate poisoning (acetylcholineeserase
inhibitor). will have cholinergic excess so atropine can reverse. but first remove all
clothes which may be soaked in the poison to prevent transcutaneous absorption.
 treat cat bites prophylactically with amoxicillin/clavulanate. pasteurella
multicoda is resistant to erythromycin 50% of the time
 heat stroke is temp > 40.5C / 105F. will have hot, dry skin and hypotension.
tachycardia, tachypnea and hemoconcentration. will have multiple organ
system effects, seizures, ARDS, dic, and hepatic/renal failure can occur.
endocrine
 isoniazid causes hepatitis with similar pathological picture to viral hepatitis
(panlobular mononuclear cell infiltration and hepatic cell necrosis)
 treat symptomatic syndrome of inappropriate antidiuretic hormone (SIADH)
with hypertonic saline 0.3% (patient will be hyponatremic)
 hereditary hemochromatosis patients are vulnerable to infections of Listeria
monocytogenes, Yersinia enterocolitica, and Vibrio vulnificus
 corticosteroids have mineralocorticoid like effects (hypokalemia, alkalosis,
hypernatremia)
 in psychogenic polydipsia, water deprivation will increase urine
concentration, but in diabetes insipidus (DI) the water will not concentrate (ADH
is not functioning). The next step is to administer ADH and if it concentrates urine
then the patient has central diabetes insipidus, if the urine is still not
concentrated then the patient has nephrogenic diabetes insipidus.
 hyperthyroidism can have rapid bone loss if left unreated. The patient will
have increased ALP
 aromatase deficiency leads to high testosterone, no estrogen, and
virilization of females. A patient with congenital adrenal hyperplasia (CAH) will
still have estrogen. Aromatase converts testosterone into estrogen.
 chronic supraphysiological doses of glucocorticoids suppress CRH from
hypothalamus. After removal of iatrogenic corticosteroids the HPA axis takes a
few months to recover.
 MEN1 parathyroid, pituitary, pancreatic (insulinoma, glucagonoma).
MEN2a medullary thyroid, pheochromocytoma, parathyroid.
MEN2b/3 medullary thyroid, pheochromocytoma, mucosal neuromas. All are
associated with the RET oncogene
 best test for Addison’s is cosyntropin stimulation test. Addison's presents
with weakness, fatigue, depression, increased pigmentation (due to
increased ACTH). Causes of addrenal insufficiency 1) diseased adrenal gland 2)
pituitary not releasing ACTH 3) decreased CRH by hypothalamus
 diabetes mellitus causes ischemic nerve damage. somatic nerve
oculomotor/CN3 - leads to “down and out”.
 factitious thyrotoxicosis is caused by ingestion of exogenous thyroid,
causing the thyroid gland to atrophy.
 if urine osmolality < 300 (low conc, lots of water) then you have complete
diabetes insipidus. partial diabetes insipidus is urine osm between 300-600.
patients with psychogenic polydipsia have hyponatremia, and diabetes insipidus
presents with hypernatremia.
 The 3 main categories of diabetic retinopathy are 1) simple – microaneurysms,
hemorrhages, exudates, retinal edema 2) pre-proliferative – cotton wool spots
3) proliferative – neovascularization
 A pituitary adenoma < 10 mm is a microadenoma. if it’s a prolactinoma, will
have bilateral galactorrhea and amenorrhea. use cabergoline/bromocriptine
which are dopamine agonists.
 diabetic nephropathy starts with increased GFR and microalbuminuria. once
you have > 300mg protein/day you have macroproteinuria and the only
intervention to reduce the decline in GFR at this point is intensive blood
pressure control. intensive glycemic control only lowers the progression to
microalbuminuria.
 hypothyroidism is associated with myopathies including elevated serum CK,
myalgias, muscle hypertrophy, proximal myopathy, rhabdomyolysis.
 tricyclic antidepressants are drugs of choice for diabetic neuropathy. But
because they can worsen urinary symptoms and give orthostatic hypotension you
can use gabapentin as a backup.
 sick euthyroid syndrome is when a patient has abnormally low T3 in acute, severe
illness.
 diabetic neuropathy can lead to a denervated bladder leading to overflow
incontinence. The patient will present with urinary frequency, nocturia, frequent
leakage of small volumes of urine and the post residual volume will be high.
 renal failure gives hypocalcemia, hyperphosphatemia, and increased
parathyroid hormone levels. The GFR falls and kidneys retain phosphate
causing hypocalcemia, leading to hyperparathyroidism.
 TSH-secreting pituitary adenomas can cause a goiter due to the effect of TSH on
the growth of the thyroid follicles. The patiente won’t have extrathyroidal
manifestations of Grave’s such as infiltrative opthalmopathy and pretibial
myxedema.
 conn’s syndrome (hyperaldosteronism) causes hypertension, mild
hypernatremia, hypokalemia, and metabolic alkalosis (excreting more acids).
 “popullary” (papillary) carcinoma is the most common thyroid malignancy.
 propylthiouracil and methimazole can cause agranulocytosis. If the patient
presents with fever, sore throat, stop anti-thyroid drug and do a CBC. if wbc <
1000 permanently stop drug.
 insulin resistance for patients with central type obesity is a key pathogenic factor
in the development of type 2 diabetes mellitus and associated abnormalities.
 Grave’s opthalmopathy is due to autoimmune lymphocytic infiltration of the
extraocular muscles resulting in fibroblast proliferation, hyaluronic acid
deposition, edema and fibrosis
 DHEA-S is produced by the adrenal glands only. DHEA, androstenedione, and
testosterone are made by the ovaries and the adrenals. Use to differentiate
between
 secondary (central) hypogonadism has low testosterone and
inappropriately normal gonadotropin levels (FSH/LH). measure serum prolactin
levels, prolactin inhibits the release of GnRH.
 the most specific test for making a diagnosis of acromegaly is to measure
growth hormone levels following an oral glucose load. IGF-1 is a good
screening test for acromegaly (IGF-1 will be increased in acromegaly), but it is
an indirect measure of GH, and other diseases can lead to decreased IGF-1 levels.
 normal saline is the initial fluid of choice in a hypotensive, dehydrated
patient with diabetes insipidus. hypotonic fluids can be started once the
intravascular volume improves.
 glucagonoma has a triad of 1) hyperglycemia 2) necrotizing dermatitis 3)
weight loss. the skin lesion is called necrolytic migratory erythema.
 diabetic patients develop neuropathy. when the small colon is involved it usually
causes diarrhea due to bacterial overgrowth, involvement of the large colon
causes constipation, involvement of the stomach causes gastroparesis,
which commonly presents as anorexia, nausea, vomiting, and abdominal bloating
and early satiety. treat with metoclopramide, bethanecol or erythromycin.
 MEN2a consists of medullary carcinoma of the thyroid, hyperparathyroidism, and
pheochromocytoma. the serum calcitonin level is elevated in patients with
medullary thyroid cancer.
 paraneoplastic Cushing’s syndrome is caused by ectopic ACTH production
by small cell lung carcinoma. It is not suppressed by dexamethasone and you
get clinical features of hyperpigmentation in sun exposed areas (skin, scars,
palmar creases, inner surface of lips, and/or buccal mucosa), easy bruising,
truncal obesiy, moon facies, buffalo hump, striae, hypertension, fatigue, glucose
intolerance, osteopenia, weakness, edema, electrolyte disturbances.
 dizziness, palpitations, trembling and sweating with exercise are
consistent with hypoglycemia in patients who take insulin and exercise
intensely.
 Cushing’s syndrome is caused by high levels of glucocorticoids/cortisol. proximal
muscle weakness, obesity, easy bruising, oily skin, acne, hirsutism.
 treat diabetic ketoacidosis with 1) aggresive rehydration, 2) insulin therapy and 3)
potassium repletion.
 The most effective treatment in slowing progression of diabetic nephropahy is
maintaining a blood pressure of < 130/80 with ACEis or ARBs.
 Cushing’s syndrome causes secondary hypertension, hyperglycemia
(cortisol activates glucagon), hypokalemia, psychiatric problems (sleep,
depression, psychosis).
 neurogenic arthropathy or charcot’s joint is a complication of neuropathy
and repeated joint trauma.
 pseudohypoparathyroidism has low serum calcium, high serum
phosphate, and high serum PTH. (calcium and phosphate levels are as if PTH
levels are low, but PTH levels are elevated)
X-linked hypophosphatemic rickets have low serum phosphate due to
renal phosphate wasting.
 patients with generalized resistance to thyroid hormones have high serum
T4 and T3 levels with normal to mildly elevated TSH. patients have features
of hypothyroidism despite having elevated free thyroid hormones.
subclinical hypothyroidism is characterized by mildly elevated TSH and
normal circulating thyroid hormones. These patients do not have features
of overt hypothyroidism.
 hyperlipidemia, unexplained hyponatremia, and elevated serum muscle
enzymes are indications for thyroid function tests.
 somogyi effect occurs when counterregulatory hormones react to nocturnal
hypoglycemia (too much insulin), thereby resulting in early morning
hyperglycemia. the patient will have low serum glucose at 3:00 AM. in the
dawn phenomenon the patient will have an increased 3:00 am glucose
concentration because of the secretion of nocturnal growth hormone.
 hemosiderosis is the deposition of excessive iron to tissues. caused by a variety
of inherited metabolic disorders. not considered to be a distinct disease
entity. hemochromatosis is an autosomal recessive disorder characterized by
increased skin pigmentation, diabetes, cirrhosis, and arthralgia
(pseudogout) in the later stages. treatment is phlebotomy for 2-3 years to
deplete iron stores, and deferoxamine as a 2nd line treatment.
 plasma aldosterone to plasma renin activity ratio (PARA) is used as an initial
screening test for primary hyperaldosteronism. a ratio > 30 is suggestive of
the diagnosis.
 hyperpigmentation of the skin and mucous membranes is characteristic of
primary adrenocortical deficiency, and is due to increased levels of ACTH.
this feature is not seen in secondary adrenal insufficiency due to
hypothalamo-pituitary failure. glucocorticoid deficiency presents as
weakness, fatigue, depression, irritability, hypotension, lymphocytosis,
neutropenia, and eosinophilia. hypothyroidism presents as cold intolerance,
constipation, dry and rough skin, bradycardia. mineralocorticoid deficiency
presents as hypokalemia, alkalosis, and mild hypernatremia.
 when you find a thyroid nodule, first do serum TSH. if serum TSH is low, do
radionuclide thyroid scan. if hyperfunctioning then evaluate for
hyperthyroidism. if non-functioning nodule then do diagnostic ultrasound
of thyroid. if nodule is suspicious for malignancy do FNA of nodule. if the
FNA is benign, routine follow up and surveillance. if TSH is normal or high then
do ultrasound of nodule. Steps: 1) TSH, 2) radionuclide scan, 3) ultrasound, 4)
FNA
 hypothyroidism leads to accumulation of matrix substances throughout the
body. if this occurs in the median nerve and the tendons of the carpal tunnel then
it may cause carpal tunnel syndrome.
 treat diabetic ketoacidosis by giving iv normal saline followed by regular
insulin, and potassium.
 hypertension in patients with thyrotoxicosis is predominantly systolic and
caused by hyperdynamic circulation. increased target organ sensitivity to
endogenous catecholamines by increasing the expression of adrenergic
receptors as well.
 subacute lymphocytic (painless) thyroiditis can cause thyrotoxicosis with
reduced radioactive iodine uptake. other causes of thyrotoxicosis with
reduced radioactive iodine uptake include: subacute granulomatous (de
quervain) thyroiditis, iodine-induced thyroid toxicosis, levothyroxine
overdose, struma ovarii.
 hyperthyroidism and hypothyroidism can cause proximal muscle
weakness. look for additional symptoms of thyroid dysfunction (fatiguability,
tremor, anxiety, weight changes, menstrual)
epidemiology
 matching is frequently used in case-control studies because it is an efficient
method to control confounding.
 a two sample t-test is a statistical method commonly used to compare the means
of two groups of subjects. ANOVA is used to compare three or more means.
 cohort study is a study done based on presence/absence of risk factors.
 Number needed to treat = 1/absolute risk reduction
 the correlation coefficient shows the strength and direction (positive or
negative) of linear association between two variables, but it doesnt imply
causality.
 a factorial design uses 2 or more experimental interventions each with 2 or more
variables that are studied independently. (wtf??)
 in a cross-sectional study, exposure and outcome are measured simultaneously at
a particular point of time (snapshot study).
 if the outcome of a case-control study is not common in the population, the odds
ratio is close to the relative risk.
 the p value is the probability that the result of a study was obtained by chance
alone. a study is statistically significant when the p value is < 0.05 (lower p value
is less due to “chance”)
 case control studies are also known as retrospective studies. researcher begins
with a population with a certain outcome and subjects are classified as cases or
controls based on outcome status. a retrospective cohort study starts at some
point between the exposure and outcome. the researcher reviews past records,
classifies subjects as “exposed” and “not exposed’ and follows them until the
outcome.
 use tests with high sensitivity to screen for diseases. (ELISA for HIV). specificity to
confirm (western blot). sn-out. sp-in
 chi-square test is used to compare proportions.
 precision is the measure of random error. the tighter the confidence interval, the
more precisde the result. increasing the sample size increases precision.
 PPV depends on prevalence of disease. NPV also depends on the prevalence of
disease, but has an inverse association with the prevalence. as prevalence of
disease increases, NPV will decrease.
gastroenterolog
y
 chronic pancreatitis can lead to pancreatic cancer. To look for pancreatic cancer
do a ct scan abdomen
 zinc def has alopecia, abnormal taste, bullous pustulous lesions, and can
occur in total paraenteral nutrition or malabsorption
 acute iron intoxication has 5 phases. 1) gastrointestinal phase- nausea, vomiting,
hematemesis, melena, abdominal pain 2) asymptomatic 3) shock and metabolic
acidosis 4) hepatotoxicity 5) mucosal scarring leading to bowel obstruction
 calcium channel blockers and nitrates relax myocytes in esophagus. relieves
diffuse esophageal spasm. diagnose with manometry
 hepatic hydrothorax is a transudative pleural effusion in a patient with
cirrhosis. salt restriction and diuretics, and then TIPS
 crohn's disease has non-caseating granulomas (pathognomonic for CD).
ulcerative colitis does not.
 GI, lung, breast generally mets to liver. prostate mets to pelvic lymph nodes.
 non-bleeding varices treated with beta-blockers. decreases risk of bleeding
by ½
 bowel ischemia and infarction is an early complication of aaa repair.
pseudomembranous colitis takes 4-5 days after antibiotic use to develop.
ischemic colitis will show thickening of the bowel wall on CT.
 in a patient with acute pancreatitis, check for underlying cause (gallstones) do
RUQ ultrasound
 inflammatory bowel disease also occurs w/ inflammatory arthritis.
ankylosing spondylitis is an association. +P-anca and also erythema nodosum
 biliary colic caused by ingestion of fatty meals. gall bladder contracts and presses
gallstone against cystic duct opening, increasing gall bladder pressure, causing
distension and colicky pain. gall bladder relaxes and stone falls back in duct.
Biliary colic is temporary, cholecystitis is more constant pain.
 pyloric stricture (and gastric outlet obstruction) lead to early satiety,
succussion splash, non bilious vomiting.
 acute appendicitis should have immediate surgery if clinical diagnosis is clear
 hematochezia is bright red blood per stool. usually due to lower gastrointestinal
bleed. do colonoscopy, if negative then do labeled erythrocyte
scintigraphy.
 laxative abuse on biopsy will show dark brown discoloration of colon with
lymph follicles shining through as pale patches (melanosis coli)
 H. pylori is associated with gastric lymphoma/MALToma but not
adenocarcinoma. once diagnosis of cancer is made, next step is to find extent
of disease.
 inflamm bowel disease has a bi-modal distribution. erythematous mucosa
possibly w/ ulcers. ulcerative colitis has shallow ulcers compared to crohn's
transmural.
 persistence of HbsAg in serum for 7 months confirms diagnosis of chronic hep b
infection. for acute hepatitis use LFTs and serology but for chronic hepatitis do
liver biopsy.
 acalculous cholecystitis is seen in severe trauma, ischemia, post-op
patients. similar to cholecystitis with thickening of gall bladder wall, and
pericholecystic fluid.
 drug induced esophagitis caused by potassium chloride, NSAIDs,
alendronate, doxycycline.
 mechanical small bowel obstruction presents with abdominal discomfort,
vomiting, abdominal distention, constipation, dilated loops of bowel on
x-ray. most commonly b/c of adhesions from previous operations.
 painless jaundice + conjugated hyperbilirubinemia + elevated ALP should raise
concern for intraabdominal malignancy that is obstructing the biliary system –
pancreatic adenocarcinoma
 chronic pancreatitis is diagnosed with stool elastase. serum amylase and
lipase concentrations can be normal or only modestly elevated.
 acute diverticulitis is uncomplicated (75%) or complicated (25%). complicated
can lead to an abscess, if < 3 cm then treated with iv antibiotics. but if
fluid collection > 3 cm then should be percutaneously drained via CT
guidance. if drain doesn’t work in 5 days then debridement and surgical drainage
can be attempted.
 for hepatic encephalopathy use lactulose, neomycin or rifamixin, and laxatives.
 sudden onset epigastric pain with air under diaphragm indicates perforated
peptic ulcer. can have diffuse abdominal pain due to peritonitis.
 primary biliary cirrhosis has symptoms of xanthelasma, pruritis, jaundice,
steatorrhea, hepatosplenomegaly, increased ALP and serum bilirubin, and +antimitochondrial
antibody. Due to destruction of the bile ducts in the portal triad.
Treat with ursodeoxycholic acid.
 lactose intolerance has a +hydrogen breath test, +stool test for reducing
substances, low stool pH and increased stool osmotic gap.
 new onset diabetes mellitus = hemochromatosis (“bronze diabetes”).
they can also have damage to liver, pituitary. will present with hepatomegaly,
hyperpigmentation, arthropahy, restrictive heart failure, and
hypogonadism. check iron levels.
 carcinoid syndrome triad includes 1) diarrhea, 2) flushing 3) valvular heart
disease. precursor of serotonin is tryptophan so patients can get niacin
deficiency. niacin def. presents as “the 4 Ds” diarrhea, dermatitis, dementia, and
death
 in patients with liver cirrhosis and who have esophageal varices give betablockers
to decrease the risk of variceal hemorrhage.
 hemorrhage is the most common complication of peptic ulcer. will present
as hematemesis with or without melena. if it’s massive upper gi bleeding it will
appear as hematochezia (bright red blood in stool).
 boerhaave’s syndrome is spontaneous rupture of the esophagus when
intraabdominal pressure goes high. retrosternal pain and crepitus in the
suprasternal notch are the result of pneumomediastinum which can occur
after rupture of esophagus within the mediastinum.
 duodenal ulcer presents with epigastric pain better upon eating. 90% infected
with h. pylori so give ppi + antibiotics
 echinococcus granulosus causes hydatid cyst disease which appears as
eggshell calcifications on CT scan of liver.
 emphysematous cholecystitis is a form of acute cholecystitis that arises due
to infection of gall bladder wall with gas forming bacteria. RUQ pain,
nausea, vomiting, low fever. diagnosis with abdominal XR demonstrating air
fluid levels in gall bladder or an ultrasound showing curvilinear gas
shadowing in the gall bladder.
 if have patient with migratory thrombophlebitis/Trousseau syndrome try to find
occult tumor.
 GERD is present in up to 75% of asthma patients. patients with adult-onset
asthma and symptoms that are worse after meals, exercise, or laying down are
likely to have gerd-induced disease. give ppi
 patients with pernicious anemia have 1) antibodies to intrinsic factor
decreasing b12 absorption and 2) atrophic gastritis with decreased production
of intrinsic factor by parietal cells. atrophic gastritis increases the risk of
intestinal-type gastric cancer and gastric carcinoid tumors.
 do anoscopy in a patient with no risk factors for colon cancer who has minimal
bright red blood per rectum
 metoclopramide is a prokinetic agent used to treat nausea, vomiting,
gastroparesis. should be monitored closely for development of drug-induced
eps (dopamine antagonist)
 in a patient with complicated GERD (gerd + weight loss, odynophagia, bleeding)
do esophagoscopy.
 vitamin d overdose gives you hypercalcemia. constipation, abdominal pain,
polyuria, polydipsia are signs of hypercalcemia.
 celiac sprue causes iron deficiency anemia, and is associated with
dermatitis herpetiformis. intensely burning, pruritic papulovesicular skin
disease. granular IgA deposits in upper dermis so test for IgA anti-endomysial
antibodies and IgG/IgA anti-gliadin antibodies.
 clues for liver mets from the colon can be: abdominal pain, mildly elevated liver
enzymes, and firm hepatomegaly. microcytic anemia due to occult
gastrointestinal bleeding, and a right sided pleural effusion caused by
hepatic hydrothorax due to cirrhosis. do a CT of the abdomen with iv contrast
to evaluate for malignancy.
 females are more susceptible to hepatic injury than males from alcohol ingestion.
alcoholic cirrhosis has an increased ratio of AST > ALT 2:1
 vanishing bile duct syndrome is a rare disease involving progressive
destruction of the intrahepatic bile ducts. primary biliary cirrhosis causes
ductopenia in adults and is characterized by the same pattern of liver injury.
 spontaneous bacterial peritonitis should be suspected in any patient with
cirrhosis and ascites who presents with low-grade fever, abdominal
discomfort or altered mental status. paracentesis with pmn > 250 and
+culture confirms diagnosis.
 pharyngoesophageal (zenker’s) diverticulum develops immediately above
the upper esophageal sphincter by herniating posteriorly between the fibers of
cricopharyngeal muscle. motor dysfunction and incoordination are responsible for
this problem. the surgical treatment of this disorder includes excision and
frequently cricopharyngeal myotomy.
 a choledochal cyst is a congenital abnormality of the biliary ducts
characterized by the dilatation of intra or extra-hepatic biliary ducts or
both. in children in can cause abdominal pain, jaundice, and attacks of
recurrent pancreatitis, which may be evident by increases in