Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MS3 > Internal Med 8 > Flashcards

Internal Med 8 Flashcards

1
Q

How do you determine if there is a coexisting metabolic disorder on top of pre-existing anion gap metabolic acidosis

A

• Determine the difference between calculated anion gap (Na – Cl – HCO3) and normal anion gap (12)
o This is how many extra H+ ions there are
o So you add this number to the measured bicarb to get “corrected” bicarb
o If corrected bicarb is greater than normal bicarb (24), you have a coexisting metabolic alkalosis
o If corrected bicarb is less than normal bicarb (24), you have a coexisting metabolic acidosis

o Example: Na = 140, Cl = 100, Bicarb = 10
♣ Anion gap = 30
♣ Difference between calculated anion gap and normal = 30 – 12 = 18
♣ Add 18 to bicarb to get “corrected” = 10 + 18 = 28
♣ Corrected bicarb is > normal bicarb of 24, so there is a coexisting metabolic alkalosis on top of this metabolic acidosis

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

Alternative tx of Syphilis if pt is allergic to Penicillin

A

Doxycycline

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

What is Whipple disease

A

♣ Infection with Tropheryma whipplei
♣ Symptoms: Weight loss, lymphadenopathy, hyperpigmentation, cardiac symptoms, arthralgias, neurologic symptoms
♣ Histology: Periodic acid Schiff, PAS (+) foamy macrophages in intestinal lamina propria

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

What would you expect to see on blood gas of a pt with asthma exacerbation

A

Respiratory alkalosis due to hyperventilation leading to decreased PaCO2

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

What would you expect to see in respiratory collapse of a pt with asthma exacerbtion who is unable to meet demands of increased respiratory drive

A

You will see a normal pH and PaCO2

Inability to maintain adequate ventilation caused by respiratory muscle fatigue or severe air trapping

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

What abx are used against Anaerobes (think of each category discussed by Jacob)

A
  • Amox/Clav
  • Amp/Sul
  • Pip/Taxo
  • Metronidazole
  • Clindamycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What abx are used against resistant GNR/Pseudomonas

A
  • Pip/Tazo
  • Cefepime
  • Imipenem
  • Meropenem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What abx are used against resistant GPC (MRSA)

A
  • Vancomycin
  • Linezolid
  • Daptomycin
  • TMP/SMX
  • Doxy
  • Clindamycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What abd are used against atypicals

A
  • Azithromycin

- Doxy

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

What is empiric tx of endocarditis

A

Vancomycin

  • It will treat against main culprits: staph, strep, and enterococcus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What drug do you use for Vancomycin-resistant enterococci

A

Daptomycin

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

Describe what absorption of D-xylose / urinary excretion indicates

A

Can be used to assess for Celiac disease
o D-xylose is a monosaccharide that is aborobed in the small intestine without degradation by pancreatic or brush border enzymes
o Patients with small intestinal mucosal disease will have impaired absorption of D-xylose, and thus decreased urinary excretion of D-xylose
o Patients with malabsorption due to enzyme deficiencies (e.g. pancreatitis), will have normal absorption of D-xylose

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

What is contraction alkalosis?

A

o Although excess alkali are filtered in the glomerulus, they are also reabsorbed as a result of an activated RAAS
o Hypovolemia triggers RAAS in an attempt to conserve sodium and water
o Aldosteron functions to retain water at the expense of excreting both potassium and acid in the urine, despite total body acid depletion (contraction alkalosis)

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

How does Lithium cause nephrogenic DI

A

Lithium antagonizes the action of ADH in the collecting tubules, which means that aquaporins don’t get put into the collecting duct

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

How do you treat nephrogenic DI secondary to Lithium

A

Amiloride

• Lithium enters the convoluted tubule via the ENac channel, so inhibiting this channel will inhibit lithium entering, so Lithium can no longer antagonize the effect of ADH

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

What will you see in the setting of abrupt withdrawal of exogenous steroids in:

  • Cortisol
  • ACTH
  • Aldosterone
A

This is tertiary adrenal insufficiency (problem of the hypothalamus)

  • Low cortisol
  • *Low ACTH
  • Normal Aldo (controlled by RAAS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe cause of common variable immunodeficiency (CVID)

A

o Defect in B-cell differentiation
♣ B cell count is normal
♣ Plasma cells and all immunoglobulins are decreased

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

Manifestations of CVID

A

♣ Recurrent respiratory (e.g. pneumonia, sinusitis, otitis) and GI (e.g. Salmonella, Campylobacter) infections
♣ Autoimmune disease (e.g. RA, thyroid disease)
♣ Chronic lung disease (e.g. bronchiectasis)
♣ GI disorders (e.g. chronic diarrhea, IBD-like conditions)

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

Tx of CVID

A

♣ Immunoglobulin replacement therapy

20
Q

Describe the autoimmune target/histology in Pemphigus Vulgaris vs. Bullous Pemphigoid

A

Pemphigus vulgaris
- Autoimmune destruction of desmosomes (connection between cells of the stratum spinosum)
• Basal layer remains attached “tombstone” appearance
• Immunofluorescence will have a fish net appearance IgG and C3 deposits in a “chicken wire” pattern

Bullous Pemphigoid
♣ Autoimmune (IgG) destruction of hemidesmosomes (connection between basal cell layer and basement membrane)
• Basal layer detached from basement membrane
• Immunofluorescence will be in a linear pattern IgG along basement membrane

21
Q

Describe clinical presentation of Pemphigus Vulgaris vs. Bullous Pemphigoid

A

Pemphigus Vulgaris
• Flaccid bullae and ulcers
• (+) Nikolsky sign (separation of epidermis upon manual stroking of skin) thin-walled bullae that rupture easily
• Oral mucosa involved

Bullous pemphigoid
♣ Tense bullae do not rupture easily (- Nikolsky sign)
♣ Oral mucosa NOT involved

22
Q

Empiric tx of outpatient CAP

A 
o	Macrolide (e.g. Azithromycin) or doxycycline (healthy)
o	Fluoroquinolone or beta-lactam + macrolide (comorbidities)
23
Q

Empiric tx of inpatient non-ICU CAP

A 
o	Fluoroquinolone (IV) – respiratory fluoroquinolones = Levofloxacin, Moxifloxacin
o	Beta-lactam (e.g. Ceftriaxone) + macrolide (IV)
24
Q

Empiric tx of inpatient ICU CAP

A

o Beta-lactam + macrolide (IV)

o Beta-lactam + fluoroquinoloe (IV)

25
Q

What lab value can differentiate between folate and B12 deficiency

A

Methylmalonic acid

Will be high in B12 deficiency and nl in folate def

26
Q

Causes of B12 deficiency

A
  • Strict long-term veganism
  • Pernicious anemia
  • Crohn’s
  • Pancreatic insufficiency
  • Gastric bypass
27
Q

Describe how pernicious anemia causes B12 deficiency

A

o B12 deficiency due to autoimmune destruction of gastric mucosa (parietal cells in the stomach), which leads to IF deficiency
♣ Recall that parietal cells produce intrinsic factor, which is necessary for B12 absorption

28
Q

How does Crohn’s cause B12 deficiency

A

o Damage to terminal ileum (e.g. Crohn’s) site of absorption

29
Q

Describe how you find out if B12 deficiency is due to poor nutrition or due to malabsorption

A

Schilling test = Determines if cause of B12 deficiency is due to poor nutrition or poor absorption
o Give pt IM injection of B12 to saturate liver
o Then give pt oral B12 and check urine
o Because body is saturated, all oral B12 will be absorbed and then excreted in the urine, so pt will have positive B12 in urine IF they were able to absorb it
♣ = deficiency due to poor nutrition
o If urine is negative for B12, that means there was poor absorption
♣ = deficiency due to malabsorption

30
Q

Causes of non-megaloblastic macrocytic anemai

A
  • Liver disease
  • Alcohol
  • Drugs (e.g. 5-fluorouracil, Zidovudine)
  • Metabolic (e.g. hereditary orotic aciduria)
31
Q

What will you see with the following in iron deficiency anemia:

  • Ferritin
  • Iron
  • %Sat
  • TIBC
A

• Low ferritin (low iron stores)
• Low serum iron
• Low % saturation (of transferrin – iron transporter)
High TIBC

32
Q

What will you see with the following in anemia of chronic disease:

  • Ferritin
  • Iron
  • %Sat
  • TIBC
A
  • High ferritin
  • Low TIBC
  • Low serum iron
  • Low % saturation
33
Q

What lab values can you use to evaluate for hemolysis vs. hemorrhage in anemia

A

In hemolysis you will see:
o Elevated LDH
o Low Haptoglobin
o Elevated T. Bili / D. Bili

34
Q

Tx of sickle cell

A

♣ Hydroxyurea – increases production of HbF

35
Q

Osmotic fragility test is positive in what disease?

A

♣ Osmotic fragility test – High percentage of lysis of RBCs in hypotonic solution

36
Q

Tx of osmotic fragility test

A

Splenectomy

37
Q

Coombs test will be positive in what anemia

A

Autoimmune hemolytic anemia

38
Q

What are the two types of autoimmune hemolytic anemia and how do you differentiate?

A 
Warm = IgG antibodies
Cold = IgM antibodies
39
Q

Describe cause of paroxysmal nocturnal hemoglobinuria

A

o Deficiency of GPI, which usually anchors DAF (CD55) to RBC membrane to protect from complement destruction
♣ Complement is activated in acidic situations
♣ Lysis occurs at night due mild respiratory acidosis

40
Q

What are the effects of ACEi on potassium

A

Lead to hyperkalemia due to decreased aldosterone levels

41
Q

Tx of sciatica

A

Usually has spontaneous resolution so initial management is relief of sx = NSAIDs and Acetaminophen

42
Q

What should you test for in a pt with pseudogout and hepatomegaly

A

Hemochromatosis (iron studies)

43
Q

What is hemochromatosis

A

o Excess iron

♣ Recessive mutation in HFE gene = abnormal iron sensing = increased intestinal absorption

44
Q

Presentation of hemochromatsosis

A

♣ Liver = elevated hepatic enzymes with hepatomegaly (early), cirrhosis (later), and increased risk of hepatocellular carcinoma
♣ Pancreas = DM
♣ Skin = bronze (due to hemosiderin deposition in macrophages)
♣ MSK = arthralgia, arthropathy, and chondrocalcinosis (pseudogout)
♣ Heart = arrhythmias; dilated cardiomyopathy
♣ Testes = atrophied

45
Q

Tx of aortic dissection

A

♣ Pain control (e.g. Morphine)
♣ IV beta blockers (ot decreased LV contractility)
♣ +/- Sodium nitroprusside (if SBP >120)
♣ Urgent surgical repair for ascending dissection

46
Q

Diagnose: Periodic back pain radiating to buttocks and thighs

A

Lumbar spinal stenosis

47
Q

Diagnose: Acute back pain with unilateral radiation down sciatic nerve to foot

A

Lumbar disc herniation

MS3 (88 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions