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Review / Wrong Answers > 6/19 UWorld > Flashcards

6/19 UWorld Flashcards

1
Q

What is the different probe used for Southern and Northern blot

A

Southern blot uses a DNA probe to detect DNA sample

Norther blot uses a DNA probe to detect RNA sample

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2
Q

Describe the different locations of GLUT2 vs. GLUT4 and whether or not they are insulin-dependent

A
  • GLUT2
    • Present on regulatory cells (liver, kidney, pancreas)
    • Insulin independent
  • GLUT4
    • Present on skeletal muscle and adipose tissue
    • Insulin dependent
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3
Q

Glucokinase:

  • Location
  • Vmax
  • Km
A

Located on cells that regulate glucose (liver and b-pancreas)

High Km = low glucose affinity; need a lot of glucose present in order for it to work (this makes sense because if glucose is low you don’t want it in regulatory cells, you want it out and being used)

High Vmax = once it is used, it works very quickly

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4
Q

Hexokinase

  • Location
  • Km
  • Vmax
A

Located on all cells

Low Km (higher glucose affinity)

Low Vmax (works slower)

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5
Q

What is the rate-limiting enzyme for glycolysis and gluconeogenesis

A

Glycolysis = phosphofructokinase I (PFKI)

Gluconeogenesis = fructose-1,6-bisphosphatase

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6
Q

What substrates enhance and inhibit PFKI

A

Enhanced by energy depleted substrates = AMP, F26BP

Inhibited extra energy cycles = by ATP and citrate

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7
Q

What substrates activate/inhbit pyruvate kinase

A

Activated by F16BP (an upstream product of glycolysis)

Inhibited by ATP and alanine

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8
Q

Describe how/where insulin and glucagon affect glycolysis/gluconeogenesis

A
  • Insulin activates PFK2, which converts F6P to F26BP
    • F26BP is an activator of glycolysis (activates PFKI) and an inhibitor of gluconeogeneis (inhibits F16BPase)
  • Glucagon activates Fructose bisphosphatase 2, which converts F26BP to F6P, which can then undergo gluconeogesis
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9
Q

What are the retroperitoneal structures

A

o SAD PUCKER

§ S à Suprarenal (adrenal gland)

§ A à Aorta and IVC

§ D à Duodenum (2nd through 4th parts)

§ P à Pancreas (except tail)

§ U à Ureters

§ C à Colon (descending and ascending)

§ K à Kidneys

§ E à Esophagus (thoracic portion)

§ R à Rectum (partially)

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10
Q

The conversion of PEP to pyruvate is irreversible. What steps/enzymes are used in gluconeogenesis to bypass this irreversible step?

A
  • Pyruvate is converted to oxaloacetate via pyruvate carboxylase (uses biotin B7)
  • Oxaloacetate converted to PEP via phosphoenolpyruvate carboxykinase (PEPCK)
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11
Q

Besides pyruvate carboxylase and PEPCK, what are the other 2 unique enzymes needed for gluconeogensis

A
  • Fructose-1,6-bisphosphatase
    • Converts F16BP to F6P
    • Rate limiting step of gluconeogenesis
  • Glucose-6-phosphatase
    • Converts G6P to glucose
    • Present only in liver and kidney (not muscle)
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12
Q

What are the 3 openings in the diaphragm

A
  • THINK: I ate ten eggs at twelve
    • I ate = “I” for IVC and “ate” for T8
    • Ten eggs = “Ten” for T10 and “eggs” for esophAGus and vAGus
    • At twelve = “At” for AAT (Aorta, Azygous, Thoracic) and twelve for T12
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13
Q

What nerve innervate the diaphragm

A
  • Diaphragm is innervated by C3, C4, and C5
    • THINK: C3, 4, 5, keeps the diaphragm alive
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14
Q

Label the lung volume graph

A
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15
Q

What lung volumes make up vital capacity

A

Everything except for residual volume (inspiratory reserve + tidal volume + expiratory reserve)

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16
Q

What lung volumes make up functional residual capacity

A

Expiratory reserve + residual volume

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17
Q

In healthy individuals, is the amount of O2 recieved perfusion-limited or diffusion-limited

A

Perfusion-limited

  • Gas equilibrates along the length of the capillary, and increased O2 can only occur via increased blood flow

Vs. diffusion-limited in emphysema and fibrosis

  • Gas does not equilibrate by the time blood reaches the end of the capillary
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18
Q

What values define pulmonary HTN

A
  • Pulmonary arterial pressure > 25 at rest (normal = 10 mm Hg)
  • Pulmonary arterial pressure > 35 during exercise
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19
Q

Differentiate between R and T forms of Hb

A
  • Taut (T) form
    • Low O2 affinity – deoxygenated
    • THINK: Taut in Tissues
  • Relaxed (R) form
    • High O2 affinity – oxygenated
    • THINK: Relaxed in respiratory area
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20
Q

Is there a R-shift or L-shift of curve in carboxyhemoglobin

A

L-shift

  • Hb bound to O2 is decreased because it is bound to CO instead = the height of curve is lower
    • Decreased O2 content in the blood
  • The heme groups NOT bound to CO have increased affinity for O2 = L shift of curve
    • This makes it more difficult for O2 to be unloaded in tissues
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21
Q

Clinical presentation of carboxyhemoglobin vs. methemoglobin

A
  • Carboxy hemoglobin
    • Headaches, dizziness, and cherry red skin
  • Methemoglobin
    • Cyanosis
    • Chocolate-colored blood
22
Q

What is the alveolar gas equation

A
  • Amount of O2 in the alveoli = amount of O2 in inspired air – amount of O2 consumed
    • pAO2 = pIO2 – (paCO2 / R)
      • pAO2 = alveolar pO2
      • pIO2 = pO2 in inspired air
      • paCO2 = arterial pCO2
    • pAO2 = 150 – (paCO2 / 0.8)
23
Q

What is the value of a normal A-a gradient

A
  • Normal = 10-15 mm Hg
  • Increased A-a gradient means that there is a problem with O2 equilibrating between alveoli and arteries:
    • Shunting or V/Q mismatch
    • Fibrosis (thickened diffusion barrier)
    • Increased FiO2 (increases pAO2 by flooding alveoli with O2, but there is still a limit as to how much O2 can go into the arteries)
    • Age
24
Q

Causes of hypoxemia that result in normal A-a gradient

A
  • Normal A-a gradient (low pAO2 and low paO2)
    • High altitude
    • Hypoventilation
25
Q

Causes of hypoxemia that result in high A-a gradient

A
  • High A-a gradient (normal pAO2 and low paO2)
    • Pulmonary fibrosis
    • R-to-L cardiac shunt (blood bypasses pulmonary vasculature and does not get oxygenated)
    • V/Q mismatch
26
Q

EKG changes in PE

A
  • EKG changes:
    • SIQ3T3 = wide S in lead I, large Q and inverted T in lead III
27
Q

What are the lab values seen in a PE (pO2, pCO2, and pH)

A

Low pO2 – due to PE

Low pCO2 – due to compensatory hyperventilation (respiratory alkalosis)

High pH – due to low pCO2

28
Q

Adverse effects of amniotic fluid embolism

A
  • Can lead to DIC, especially postpartum
29
Q

In CO poisoning, what will you see in paO2, saO2, and oxygen content?

A

SaO2 = decreased (CO competes with O2)

PaO2 = normal

Total oxygen content = decreased

30
Q

In polycythemia, what will you see in paO2, saO2, and oxygen content?

A

PaO2 = normal

SaO2 = normal

Total O2 content = increased

31
Q

In anemia, what will you see in paO2, saO2, and oxygen content?

A

Oxygen content will be decreased because hemoglobin is decreased

SaO2 measures the saturation of the hemoglobin that you do have, so it won’t change since the remaining hemoglobin will be normally saturated

PaO2 measures O2 dissolved in blood, which has nothing to do with Hb, so will also be normal

32
Q

What is detection bias

A

· Refers to the fact that a risk factor itself may lead to extensive diagnostic investigation and increase the probability that a disease is identified

· E.g. smokers may undergo increased imaging surveillance due to smoking status, which would detect more cases of cancer in general

33
Q

Enzyme deficiency and presentation of von Gierke

A
  • Deficient glucose-6-phosphatase
  • Causes a defect in both glycogenolysis and gluconeogenesis
  • Presentation:
    • Severe fasting hypoglycemia, lactic acidosis, hepatomegaly & steatosis, hyperuricemia & hyperlipidemia
34
Q

Enzyme deficiency and presentation of Pompe

A
  • Deficient in lysosomal alpha-1,4-glucosidase
    • Enzyme usually degrades small amounts of glycogen trapped in lysosomes
    • Enzyme deficiency leads to glycogen accumulation within lysosomes (appears as periodic acid-schiff-positive material
  • Presentation:
    • Normal glucose levels
    • Cardiomegaly, hypertrophic cardiomyopathy, exercise intolerance, hypotonia
      • THINK: Pompe = fat = symptoms of obesity
    • Shortened life expectancy
35
Q

Enzyme deficiency and presentation of Cori disease

A
  • Deficient in debranching enzymes
    • THINK: Cori wants me to climb his “straight branch”
  • Causes a defect in glycogenolysis but gluconeogenesis is fine
  • Presentation:
    • o Milder version of Von Gierke disease
    • o Hepatomegaly, ketotic hypoglycemia, hypotonia and weakness, abnormal glycogen with very short outer chains
36
Q

Enzyme deficiency and presentation of McArdle Disease

A
  • Deficient in skeletal muscle glycogen phosphorylase
    • McArdle = Muscle
  • Can make glycogen but can’t break it down
  • Increased glycogen in muscle à increased osmotic pressure à swelling and lysis of myocytes à rhabdomyolysis à myoglobin in serum à myoglobin in urine (myoglobulinuria)
  • Presentation:
    • o Weakness and fatigue with exercise
    • o No rise in blood lactate levels after exercise
37
Q

Stimulation of what nerve can improve the symptoms of obstructive sleep apnea

A

Stimulation of the hypoglossal nerve using an implantable nerve stimulator causes the tongue to move forward slightly, increased the anteroposterior diameter of the airways

38
Q

Criteria of manic epidose

A
  • Lasting at least one week
  • At least one of these criteria: DIG FAST
    • D – Distractibility
    • I – Irresponsibility
    • G – Grandiosity
    • F – Flight of ideas (e.g. racing thoughts)
    • A – Goal-directed Activity / Agitation
    • S – decreased need for Sleep
    • T – Talkativeness
39
Q

MOA behind tyramine toxicity

A
  • Tyramine naturally occurring monoamine compound found in aged meats, alcoholic beverages, and fermented dairy products
  • Tyramine acts as a catecholamine releasing agent, but before it gets to the general circulation it is metabolized in the GI tract by MAO-A
  • But if you inhibit MAO-A, all the Tyramine flows in the circulation and acts as a sympathomimetic agent, displacing NE from neuronal storage vesicles
  • Tyramine toxicity can precipitate a hypertensive crisis (e.g. HTN, blurry vision, diaphoresis)
40
Q

Treatment of Phentolamine

A

Phentolamine (alpha-1 and alpha-2 antagonist)

41
Q

What is the feared complication associated with antiphospholipid antibodies

A

Hypercoagulable state

Often presents with multiple spontaneous abortions

Antibodies associated with SLE

42
Q

Symptoms associated with SLE

A
  • RASH OR PAIN
    • R – Rash (malar or discoid)
    • A – Arthritis (non-erosive, 2 joints)
    • S – Serositis (e.g. pleuritic, pericarditis)
    • H – Hematologic disorders (hemolytic anemia, leukopenia, lymphopenia, thrombocytopenia)
    • O – Oral/nasopharyngeal ulcers (painless)
    • R – Renal disease (diffuse proliferative glomerulonephritis or membranous glomerulonephritis)
    • P – Photosensitivity
    • A – Antinuclear antibodies (+ANA)
    • I – Immunologic disorder (anti-dsDNA, anti-Smith, anti-histone, or anti-phospholipid/anti-cardiolipin)
    • N – Neurologic disorders (seizures, psychosis)
43
Q

In what part of the brain do you see atrophy in Huntingtons

A

Caudate and putamen

44
Q

In what disease will you see dementia + visual hallucinations

A

Lewy body dementia

45
Q

Is BPH due to hypertrophy or hyperplasia

A

Hyperplasia

46
Q

What is Mittelschmerz

A

Transient mid-cycle ovulatory pain

Associated with peritoneal irritation

47
Q

What are the stimulators and products of theca and granulosa cells?

A
  • Theca cells
    • Stimulated by LH
    • Produce androstenedione from cholesterol via desmolase
  • Granulosa cells
    • Stimulated by FSH
    • Produce estrogen (estradiol) from androstenedione via aromatase
48
Q

Describe pathogenesis of PCOS

A
  • Increases LH = stimulation of theca cells = increased androgen production by theca cells = increased peripheral conversion of androgens into estrone in adipose tissue = decreased FSH (negative feedback) = decreased stimulation of granulosa cells = degeneration of follicles = cystic follicles
49
Q

What is the associated cause and complication of vaginal adenosis

A
  • Associated with diethylstilbestrol (DES) in utero and clear cell adenocarcinoma
  • Adenosis:
    • Persistence of columnar epithelium within the upper vagina
      • Lower 1/3 of vagina derived from urogenital sinus = squamous epithelium
      • Upper 2/3 of vagina derived from Mullerian duct = columnar epithelium
      • Normally, squamous epithelium will grow upwards to replace the columnar epithelium
50
Q

Common metastatic location of prostate cancer

A

Bone

51
Q

Serious complication of invasive cervical carcinoma

A
  • Lateral invasion can block ureters leading to hydronephrosis and postrenal failure

Review / Wrong Answers (140 decks)

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