Internal Med 10 Flashcards

1
Q

Describe the murmur of mitral stenosis

A

o Delayed rumbling mid-to-late diastolic murmur

o Follows opening snap (after S2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Effects of ACEi on potassium

A

Hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Tx of hyperalcemia

A
  • Aggressive hydration
  • Immediate : Calcitonin
  • Long-term : Bisphosphonates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe contraction alkalosis

A

Fluid depletion (hypovolemia) triggers the RAAS system = increased aldosterone = aldosterone retains water at the expense of excreting potassium and acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe presentation of vWB disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe Bernard-Soulier syndrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe Glanzmann thrombasthemia

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the purpose of a mixing study

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe Factor V Leiden disease

A

♣ Mutation that makes Factor Va resistant to inactivation by protein C
♣ Increased coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Will you be hyper or hypocoagulable in Protein C or S deficiency

A

♣ Unable to inactivate factors V and VIII = hypercoagulable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the first step in approach to hyponatremia

A

o Calculate Serum Osmols = (2 x Na) + (Gluc / 18) + (BUN / 2.8)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Next step if hyponatremia is isotonic (serum osmols = 280)

A

• Psuedo-hyponatremia

o Caused by fats and proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Next step if hyponatremia is hypertonic (>280)

A

• Na is low in order to balance out another component of the equation that is high
o Hyperglycemia
o Elevated BUN
♣ Kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Next step if hyponatremia is hypotonic (<280)

A

Determine volume status

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Next step if hypotonic hyponatremia is hypervolemic

A

o Calculate urine sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ddx for hypervolemic hypotonic hyponatremia with high urine sodium

A

• 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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Ddx for hypervolemic hypotonic hyponatremia with low urine sodium

A

• Due to low effective arterial blood volume (aka kidney is under the impression it is hypoperfused) Heart failure, cirrhosis, renal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Next step if hypotonic hyponatremia is hypovolemic

A

Calculate urine sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ddx for hypovolemic hypotonic hyponatremia with high urine sodium

A
  • Diuresis
  • Cerebral salt wasting
  • Primary adrenal insufficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Ddx for hypovolemic hypotonic hyponatremia with low urine sodium

A

• Extrarenal losses (GI loss, third spacing, diuretics)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Next step if hypotonic hyponatremia is euvolemic

A

o Calculate urine osmolality

they should all have normal urine sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Ddx for euvolemic hypotonic hyponatremia with high urine sodium

A
  • SIADH

* Severe hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Ddx for euvolemic hypotonic hyponatremia with low urine sodium

A

• Psychogenic polydipsia

24
Q

Cause of TTP

A
o	Due to decreased ADAMTS13, enzyme that normally cleaves vWF for degradation
♣	No vWF degradation = abnormal platelet adhesion = microthrombi
25
Q

Presentation of TTP

A
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)
26
Q

Diagnosis of TTP

A
♣	Smear
•	Low platelets
•	Schistocytes
♣	Get labs to check for DIC
•	PT/PTT = normal
•	Fibrinogen = normal
•	D-dimer = normal
27
Q

Describe the pathogenesis of DIC

A

o Widespread activation of clotting

o This consumes all platelets and coagulation factors, resulting in bleeding

28
Q

Describe smear of DIC

A

♣ Smear (same as TTP)
• Low platelets
• Schistocytes

29
Q

Describe labs of DIC (PT/PTT, Fibrinogen, D-dimer

A
  • PT/PTT = high
  • Fibrinogen = low (being used up)
  • D-dimer = high
30
Q

Describe pathogenesis of HIT

A

♣ 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

31
Q

Will you be hyper or hypocoagulable in HIT

A

♣ Leads to thrombocytopenia and hypercoagulable state (platelet fragments activate other platelets)

32
Q

Tx of HIT

A

♣ Stop Heparin

♣ Need to stop clots = Synthetic heparin (Leparudin or Agatroban) and bridge to Coumadin

33
Q

Describe pathogenesis of ITP

A

o IgG autoantibodies to GP2b3a

o Antibodies produced by plasma cells of spleen and antibody-bound platelets consumed by macrophages of spleen

34
Q

Tx of ITP

A

♣ Steroids and IVIG (autoimmune treatment)

♣ Splenectomy

35
Q

What are the cut-offs for positive PPD skin test

A

♣ >/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

36
Q

Next step if pt has a positive PPD

A

Get CXR

37
Q

Next step if +PPD and -CXR

A

• Latent TB

o Treat with INH + Vitamin B6

38
Q

Next step if +PPD and +CXR

A

Get AFB smear

39
Q

Next step if +PPD, +CXR, -AFB

A

♣ Latent TB

• Treat with INH + Vitamin B6

40
Q

Next step if +PPD, +CXR, +AFB

A

♣ Active TB

• Treat with RIPE therapy

41
Q

What do you do if pt has signs of CNS infection but unsafe to give LP?

A

Give abx FIRST and then get CT scan

42
Q

What will you see on CSF in bacterial meningitis

A
  • WBC > 1000
  • Neutrophlic predominance
  • Glucose < 46
  • Protein > 250
  • Gram stain positive
  • Elevated opening pressure
43
Q

Empiric tx of meningitis

A

CTX + Vanc + Steroids

44
Q

What do you add to empiric tx of meningitis if immunosuppressed

A

Ampicillin (+ CTX + Vanc + Steroids)

45
Q

Tx of necrotizing fascitis

A

CTX + Clinda + Ampicillin

46
Q

What bug should you think of for osteomyelitis in the following situations:

  • Most common
  • Sickle cell
  • Penetrating wound / sneaker
  • Diabetic foot
A
  • Most common = staph
  • Sickle cell = salmonella
  • Penetrating wound / sneaker = pseudomonas
  • Diabetic foot = pseudomonas
47
Q

Empiric tx of hospital acquired pneumonia

A

Want to cover Pseudomonas and MRSA

Pip/Tazo + Vanc

48
Q

What is the relationship between prolactin and dopamine

A

Dopamine inhibits the secretion of prolactin

49
Q

What is the relationship between prolactin and GNRH

A

Prolactin suppresses gonadotropin releasing hormone, LH, and estradiol

50
Q

Tx of prolactinoma

A

Dopamine agonists (Cabergoline, Bromocriptine)

51
Q

Tx of TTP

A

Plasma exchange transfusion

52
Q

Components of MEN1

A

♣ Pituitary tumors (prolactin or GH)
♣ Pancreatic endocrine tumors (Zollinger-Ellison syndrome, insulinomas, VIPomas, glucagonomas)
♣ Parathyroid adenomas

53
Q

Components of MEN 2A

A

♣ Medullary thyroid carcinoma (neoplasm of parafollicular C cells which secrete calcitonin)
♣ Pheochromocytoma
♣ Parathyroid hyperplasia

54
Q

Components of MEN 2B

A

♣ Medullary thyroid carcinoma
♣ Pheochromocytoma
♣ Mucosal neuromas (oral/intestinal ganglioneuromatosis) / Marfanoid habitus

55
Q

Tx of UTI in pregnancy

A

Amoxicillin