Internal Med 10 Flashcards
Describe the murmur of mitral stenosis
o Delayed rumbling mid-to-late diastolic murmur
o Follows opening snap (after S2)
Effects of ACEi on potassium
Hyperkalemia
Tx of hyperalcemia
- Aggressive hydration
- Immediate : Calcitonin
- Long-term : Bisphosphonates
Describe contraction alkalosis
Fluid depletion (hypovolemia) triggers the RAAS system = increased aldosterone = aldosterone retains water at the expense of excreting potassium and acid
Describe presentation of vWB disease
o Genetic vWF deficiency
o Findings:
♣ Increased bleeding time – decreased platelet adhesion
♣ Increased PTT – vWF normally stabilizes Factor VIII
o Treatment
♣ Desmopressin (DDAVP) – increases vWF release from Weibel-Palade bodies of endothelial cells
Describe Bernard-Soulier syndrome
No double letters so you know this is a defect in GP1
o Platelet can’t bind to vWF on collagen = defect of platelet plug formation
o Platelet count is only slightly low – moderate thrombocytopenia
o Large platelets
Describe Glanzmann thrombasthemia
Has double letters (“nn”) so you know this is a defect in GP2
o Genetic GP2b3a deficiency
o Defect in platelet aggregation
o Platelet count is normal (they aren’t being destroyed, just can’t aggregate)
What is the purpose of a mixing study
- To evaluate for hemophilias
- Will determine if it is autoimmune or just a lack of clotting factors
- Will correct with mixing study if lack of clotting factors
- Will not correct if it is autoimmune destruction
Describe Factor V Leiden disease
♣ Mutation that makes Factor Va resistant to inactivation by protein C
♣ Increased coagulation
Will you be hyper or hypocoagulable in Protein C or S deficiency
♣ Unable to inactivate factors V and VIII = hypercoagulable
What is the first step in approach to hyponatremia
o Calculate Serum Osmols = (2 x Na) + (Gluc / 18) + (BUN / 2.8)
Next step if hyponatremia is isotonic (serum osmols = 280)
• Psuedo-hyponatremia
o Caused by fats and proteins
Next step if hyponatremia is hypertonic (>280)
• Na is low in order to balance out another component of the equation that is high
o Hyperglycemia
o Elevated BUN
♣ Kidney disease
Next step if hyponatremia is hypotonic (<280)
Determine volume status
Next step if hypotonic hyponatremia is hypervolemic
o Calculate urine sodium
Ddx for hypervolemic hypotonic hyponatremia with high urine sodium
• Diuretics (this is not the cause, but this can be the presentation in a volume overloaded pt who is being diuresed and the diuretic is working hard)
Ddx for hypervolemic hypotonic hyponatremia with low urine sodium
• Due to low effective arterial blood volume (aka kidney is under the impression it is hypoperfused) Heart failure, cirrhosis, renal disease
Next step if hypotonic hyponatremia is hypovolemic
Calculate urine sodium
Ddx for hypovolemic hypotonic hyponatremia with high urine sodium
- Diuresis
- Cerebral salt wasting
- Primary adrenal insufficiency
Ddx for hypovolemic hypotonic hyponatremia with low urine sodium
• Extrarenal losses (GI loss, third spacing, diuretics)
Next step if hypotonic hyponatremia is euvolemic
o Calculate urine osmolality
they should all have normal urine sodium
Ddx for euvolemic hypotonic hyponatremia with high urine sodium
- SIADH
* Severe hypothyroidism
Ddx for euvolemic hypotonic hyponatremia with low urine sodium
• Psychogenic polydipsia
Cause of TTP
o Due to decreased ADAMTS13, enzyme that normally cleaves vWF for degradation ♣ No vWF degradation = abnormal platelet adhesion = microthrombi
Presentation of TTP
o Findings (Pentad) – THINK: FAT RN ♣ F = Fever ♣ A = anemia (Microangiopathic hemolytic anemia = RBCs sheared by microthrombi) ♣ T = thrombocytopenia (platelets being used up) ♣ R = renal insufficiency (thrombi involve vessels of kidney) ♣ N = neurological symptoms – confusion, HA, seizures, coma (thrombi involve vessels of CNS)
Diagnosis of TTP
♣ Smear • Low platelets • Schistocytes ♣ Get labs to check for DIC • PT/PTT = normal • Fibrinogen = normal • D-dimer = normal
Describe the pathogenesis of DIC
o Widespread activation of clotting
o This consumes all platelets and coagulation factors, resulting in bleeding
Describe smear of DIC
♣ Smear (same as TTP)
• Low platelets
• Schistocytes
Describe labs of DIC (PT/PTT, Fibrinogen, D-dimer
- PT/PTT = high
- Fibrinogen = low (being used up)
- D-dimer = high
Describe pathogenesis of HIT
♣ Heparin binds to platelet factor 4
♣ Antibodies form against this complex
♣ Antibody-heparin-PF4 complex can then destroy platelets, and their fragments will activate remaining platelets
Will you be hyper or hypocoagulable in HIT
♣ Leads to thrombocytopenia and hypercoagulable state (platelet fragments activate other platelets)
Tx of HIT
♣ Stop Heparin
♣ Need to stop clots = Synthetic heparin (Leparudin or Agatroban) and bridge to Coumadin
Describe pathogenesis of ITP
o IgG autoantibodies to GP2b3a
o Antibodies produced by plasma cells of spleen and antibody-bound platelets consumed by macrophages of spleen
Tx of ITP
♣ Steroids and IVIG (autoimmune treatment)
♣ Splenectomy
What are the cut-offs for positive PPD skin test
♣ >/5 mm
• HIV+ patients
• Recent contacts of known TB cases
• Nodular or fibrotic changes on CXR consistent with previously healed TB
• Organ transplant recipients or other immunosuppressed
♣ >/= 10 mm
• Recent immigrants (<5 years) from TB-endemic areas
• Injection drug users
• Residents and emplyees of high-risk settings (e.g. prisons, nursing homes, hospitals, homeless shelters)
• Mycobacteriology lab personnel
• Higher risk for TB reactivation (e.g. DM, leukemia, ESRD, chronic malabsorption syndromes)
• Children age <4, or those exposed to adults in high-risk categories
♣ >/= 15 mm
• All of the above plus healthy individuals
Next step if pt has a positive PPD
Get CXR
Next step if +PPD and -CXR
• Latent TB
o Treat with INH + Vitamin B6
Next step if +PPD and +CXR
Get AFB smear
Next step if +PPD, +CXR, -AFB
♣ Latent TB
• Treat with INH + Vitamin B6
Next step if +PPD, +CXR, +AFB
♣ Active TB
• Treat with RIPE therapy
What do you do if pt has signs of CNS infection but unsafe to give LP?
Give abx FIRST and then get CT scan
What will you see on CSF in bacterial meningitis
- WBC > 1000
- Neutrophlic predominance
- Glucose < 46
- Protein > 250
- Gram stain positive
- Elevated opening pressure
Empiric tx of meningitis
CTX + Vanc + Steroids
What do you add to empiric tx of meningitis if immunosuppressed
Ampicillin (+ CTX + Vanc + Steroids)
Tx of necrotizing fascitis
CTX + Clinda + Ampicillin
What bug should you think of for osteomyelitis in the following situations:
- Most common
- Sickle cell
- Penetrating wound / sneaker
- Diabetic foot
- Most common = staph
- Sickle cell = salmonella
- Penetrating wound / sneaker = pseudomonas
- Diabetic foot = pseudomonas
Empiric tx of hospital acquired pneumonia
Want to cover Pseudomonas and MRSA
Pip/Tazo + Vanc
What is the relationship between prolactin and dopamine
Dopamine inhibits the secretion of prolactin
What is the relationship between prolactin and GNRH
Prolactin suppresses gonadotropin releasing hormone, LH, and estradiol
Tx of prolactinoma
Dopamine agonists (Cabergoline, Bromocriptine)
Tx of TTP
Plasma exchange transfusion
Components of MEN1
♣ Pituitary tumors (prolactin or GH)
♣ Pancreatic endocrine tumors (Zollinger-Ellison syndrome, insulinomas, VIPomas, glucagonomas)
♣ Parathyroid adenomas
Components of MEN 2A
♣ Medullary thyroid carcinoma (neoplasm of parafollicular C cells which secrete calcitonin)
♣ Pheochromocytoma
♣ Parathyroid hyperplasia
Components of MEN 2B
♣ Medullary thyroid carcinoma
♣ Pheochromocytoma
♣ Mucosal neuromas (oral/intestinal ganglioneuromatosis) / Marfanoid habitus
Tx of UTI in pregnancy
Amoxicillin
