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Review / Wrong Answers > 6/19 UWorld > Flashcards

6/19 UWorld Flashcards

1
Q

What are the IV anesthetic choices

A
  • Benzos (conscious sedation for minor procedures)
  • Barbiturares (used for induction of anesthesia an short procedures)
  • Propofol
  • Etomidate
  • Ketamine
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2
Q

MOA and adverse effects of propofol

A

MOA: potentiates GABA-A

Adverse: CV effect (decreased in systolic BP)

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3
Q

MOA and adverse effects of Etomidate

A

MOA: potentiates GABA-A

Adverse effects: preserves CV stability

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4
Q

MOA and adverse effects of Ketamine

A

MOA: NMDA inhibitor

Adverse effects: CV stimulant, disorientation, hallucinations, unpleasant dreams,

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5
Q

What are the inhaled anesthetics

A

Nitrous oxide (non-volatile)

Halothane, Isoflurane, Enflurane (volatile)

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6
Q

Describe the difference in solubulity in blood, onset of action, and duration of action in volatile vs. non-volatile anesthetics

A
  • Non-volatile (N2O)
    • Less soluble in blood
    • Faster onset of action
    • Shorter duration
  • Volatile (e.g. Halothane)
    • More soluble in blood
    • Slower onset of action
    • Longer duration
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7
Q

What does blood:gas coefficient mean, and which has higher/lower - volatile or nonvolatile

A

Blood:gas coefficient = solubility in blood

Volatile anesthetics have higher blood:gas coefficient

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8
Q

What are adverse effects of all inhaled anesthetics

A

CV - mycardial depression, increased cerebral blood flow (due to decreased vascular resistance)

Respiratory depression (all inhaled anesthetics EXCEPT N2O)

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9
Q

Adverse effect specific to Halothane

A

Hepatic necrosis with 80% mortality

Halothane no longer used in US

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10
Q

Adverse effects specific to Enflurane

A

Nephrotoxicity

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11
Q

Drug causes of Malignant hyperthermia

A

VOLATILE inhaled anesthetics (not N2O) and Succinylcholine (depolarizing muscle relaxant)

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12
Q
A
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13
Q

Enzyme, substrate, and presentation of Fabry

A
  • XLR
  • Deficiency:
    • o Alpha-galactosidase
  • Accumulated substrate:
    • o Globotriaosylceramide
  • Presents with:
    • o Angiokeratoma
    • o Peripheral neuropathy
    • o Glomerulonephropathy
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14
Q
  • Enzyme, substrate, and presentation of Gaucher
A
  • AR
  • Deficiency:
    • o GLucocerebrosidase
  • Accumulated substrate:
    • o Glucocerebroside
  • Presents with:
    • o Hepatosplenomegaly
    • o Pancytopenia
    • o Bone pain/osteopenia
    • o Gaucher cell – lipid-laden macrophage with “crumpled tissue paper” appearance
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15
Q
  • Enzyme, substrate, and presentation of Tay Sachs
A
  • AR
  • Deficiency:
    • o Beta-hexoaminidase A (THINK: tay saX = heXaminidase)​
  • Accumulated substrate:
    • o GM2 ganglioside
  • Presents with:
    • o Macular cherry red spot
    • o Progressive neurodegeneration
    • o No hepatosplenomegaly
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16
Q
  • Enzyme, substrate, and presentation of Neimann Pick
A
  • AR
  • Deficiency:
    • o Sphingomyelinase​
  • Accumulated substrate
    • o Sphingomyelin
  • Presents with:
    • o Macular cherry red spot
    • o Progressive neurodegeneration
    • o Hepatosplenomegaly
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17
Q
  • Enzyme, substrate, and presentation of Krabbe disease
A
  • AR
  • Deficiency:
    • o Galactocerebrosidase
  • Accumulated substrate
    • o Galactocerebroside
    • o Psychosine
  • Presents with:
    • o Progressive neurodegeneration
    • o Peripheral neuropathy
    • o Optic atrophy
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18
Q
  • Enzyme, substrate, and presentation of Metachromatic leukodystrophy
A
  • AR
  • Deficiency:
    • o Arylsulfatase A
  • Accumulated substrate
    • o Cerebroside sulfate
  • Presents with:
    • o Progressive neurodegeneration
    • o Peripheral neuropathy
    • o Ataxia and dementia
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19
Q
  • Enzyme, substrate, and presentation of Hurler
A
  • AR
  • Deficiency:
    • o Alpha-L-iduronidase
  • Accumulated substrate:
    • o Heparin sulfate and dermatan sulfate
  • Presents with:
    • o Developmental delay
    • o Gargoylism
    • o Airway obstruction
    • o *Corneal clouding
    • o Hepatosplenomegaly
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20
Q
  • Enzyme, substrate, and presentation of Hunter
A
  • XLR
  • Deficiency:
    • o Iduronate sulfatase
  • Accumulated substrate:
    • o Heparin sulfate and dermatan sulfate
  • Presents with:
    • o Mild Hurler
    • o Aggressive behavior
    • o *No corneal clouding
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21
Q

Where are the location of B-cells, T-cells, and macrophages within the lymph node

A
  • B-cell
    • Located in follicle in the outer cortez
  • T-cell
    • Located in paracortex
  • Macrophages
    • Located in medullary sinuses
22
Q

What is located in the red pulp vs. white pulp of spleen

A

Red pulp = RBC

White pulp WBC

23
Q

Where is the location of B-cells, T-cells, and macrophages in the spleen

A

B-cells = germinal center of the follicle

T-cells = Periarteriolar lymphoid sheath (surrounding the central artery)

Macrophages = marginal zone (area between the red and white pulp

24
Q

What are the 4 possible fates of pyruvate?

A
  • Acetyl CoA via pyruvate dehydrogenase (TCA cycle)
  • Oxaloacetate via pyruvate carboxylase (gluconeogenesis)
  • Lactate
  • Alanine (urea cycle)
25
Q

Vitamins needed for pyruvate dehydrogenase complex

A

B1, B2, B3, B5, Lipoic adi

THINK: TLC For Nobody

o T – Thiamin (B1)

o L – Lipoic acid

o C – CoA (B5)

o FAD – Riboflavin (B2)

o NAD – Niacin (B3)

26
Q

What other enzyme needs the cofactors TLC For Nobody

A

alpha-keto glutarate dehydrogenase

27
Q

What substance is inhibited by arsenic and what is the presentation of arsenic poisoning

A

Arsenic inhibits lipoid acid (TLC For Nobody)

Clinical findings of arsenic poisoning: garlic breath, vomiting, rice-water stools, QT prolongation

28
Q

Differentiate between pyruvate kinase deficiency and pyruvate dehydrogenase deficiency

A
  • Pyruvate kinase deficiency
    • Cannot make pyruvate = no glycolysis = low ATP
    • Inability to maintain Na/K ATPase = RBC swelling and lysis
  • Pyruvate dehydrogenase deficiency
    • Buildup of pyruvate = lactic acidosis and neuro deficits
    • Treat with ketogenic diet (lysine and leucine)
29
Q

Rate limiting enzyme of TCA cycle

A

isocitrate dehydrogenase

30
Q

What step of the TCA cycle uses FAD+ to produce FADH2

A

Succinate –> fumarate

31
Q

What is the function of uncoupling agents

A

They uncouple the complexes of the electron transport chain from the final ATPase complex

So instead of all the H+ that was pumped into the intermembranous space passing down gradient through the ATPase to generate ATP, the H+ just diffuse across the membrane on their own (not the the ATPase) and create wasted energy = heat production

32
Q

Describe the fate of pyruvate that is converted to alanine

A
  • Pyruvate + glutamate = alanine + a-ketoglutarate
    • Via pyruvate aminotransferase
      • Aminotransferases named based on NH3 donor
  • Alanine is the nitrogen transporter that will bring NH3 to the liver to participate in the urea cycle
33
Q

What cofactor is neede for all aminotransferases

A

Pyridoxal phosphate (Vitamin B6)

34
Q

What are the 4 important functions of NADPH

A
  1. Fatty acid and steroid synthesis
  2. Generation of O2 free radicals (O2 to O2- via NADPH oxidase)
  3. Protection of RBC from O2 free radicals (via reduction of glutathionine)
  4. CYP-450 enzymes
35
Q

Describe the steps of oxygen free radical formation in phagolysosomes

A

O2 to O2- via NADPH oxidase

O2- to H2O2 via superoxide dismutase

H2O2 to HOCl via myeloperoxidase

36
Q

What is the enzyme that takes over fructose metabolism in Essential fructosuria (fructokinase deficiency)

A

Hexokinase

37
Q

Accumulated substrate and presentation of Galactokinase deficiency

A

§ Deficiency in galactokinase

§ Leads to accumulation of galacticol

§ Symptoms:

· Infantile cataracts

· Galactosemia and galactosuria

38
Q

Deficieny enzyme and presentation of Classic galactosemia

A

§ Deficiency in galactose-1-phosphate uridyltransferase

§ Symptoms:

· Infantile cataracts

· Failure to thrive

· Jaundice

· Vomiting

· Hepatomegaly

· Renal dysfunction

· Intellectual disability

· E. Coli sepsis

39
Q

What is the carb to calorie ration of protein, carbs, alcohol, and fatty acids

A

1 g carb/protein = 4 kcal

1 g alcohol = 7 kcal

1 g fatty acid = 9 kcal

40
Q

What part of the body can ONLY use glucose for fuel

A

RBC

Brain prefers glucose, but can use ketone bodies

41
Q

What is the function of HMG CoA synthase in the mitochondria vs. cytosol

A

Mitochondria = ketogenesis

Cytosol = choleserol synthesis

42
Q

Why do you get fasting hypoglycemia after ethanol consumption

A

The liver will preferentially metabolize ethanol over glucose

During ethanol metabolism, NAD+ is used up (via alcohol dehydrogenase)

In order to regenerate NAD+, the liver converts pyruvate to lactate and oxaloacetate to malate

Now there are no intermediates left to perform gluconeogenesis = fasting hypoglycemia

43
Q

Function of chylomicrons

A

Delivers dietary TG to peripheral tissues

Delivers cholesterol to liver in form of chylomicron remnants

44
Q

Function of LDL

A

Delivers depatic cholesterol to peripheral tissues

Take up by target cells via Clathrin-mediated endocytosis

45
Q

Function of Apo E

A

Mediates remnant uptake

On chylomicrons

46
Q

Function of Apo A1

A

Activates LCAT (enzyme that esterifies cholesterol within HDL that was taken up from periphery_

47
Q

Function of Apo C2

A

LPL cofactor

48
Q

Function of Apo B48

A

Mediates chylomicron secretion from enterocyte into lymphatics

49
Q

Function of Apo B100

A

Bunds LDL receptor

50
Q

Function of CETP (cholesterol ester transfer protein)

A

Transfers cholesterol esters from HDL to VLDL/LDL to be take back to the liver

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