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From Flashcardlet > 5/19 > Flashcards

5/19 Flashcards

1
Q

What drugs can effectively treat eye inflammation associated with graves disease?

A

Corticosteroids

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2
Q

What cancers are associated with EBV infection?

A

Burkitt lymphoma and nasopharyngeal cancer

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3
Q

What does the enzyme phenylethanolamine N methyltransferase (PNMT) do?

Where does this take place?

What can increase this process?

A

PNMT converts NE to Epi in the adrenal medulla

Cortisol (produced by the adrenal cortex) can increase this process

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4
Q

What class is echovirus in? What can it cause?

A

it is an eterovirus, along with coxsackievirus.

These both can cause aseptic meningitis

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5
Q

What is the cause of a palpable but nontender gallbladder, weight loss, obstructive jaundice (pruritus, dark urine, and pale stools)?

A

Pancreatic CA in the head of the pancreas - obstructs the gallbladder

Main risk factor is smoking, age, and chronic pancreatitis

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6
Q

Histology and location of a juvenile pilocytic astrocytoma

A

Usually occur in the cerbellum, brainstem, or optic pathways

Consist of spindle cells with hair like glial processes that are associated with microcysts

Also see rosenthal fibers and granular eosinophilic bodies

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7
Q

Polycistronic vs monocistronic mRNA

A

Poly = one mRNA can code for multiple proteins. Prokaryotes have lots of these

Mono = one mRNA makes one protein. This is what eukaryotes have

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8
Q

Comedocarcinoma = DCIS

A

breast cancer

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9
Q

What are the symptoms of hydrocephalus?

A

Irritability, poor feeding, increased head circumference. Can lead to visual disturbances, and learning disabilities w/ spasticity and hypertonicity of muscles due to stretching of periventricular pyramidal tracts

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10
Q

What type of defenses kill listeria?

A

Cell mediated immunity

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11
Q

What can rapid correction of hyponatremia cause?

A

Osmotic demyelination of the axons in the central pons (Central Pontine Myelinolysis –> quadriplegia and pseudobulbar palsy

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12
Q

What processes take place in both the cytoplasm and the mitochondria?

A

Gluconeogenesis

Urea Cycle

Heme Synthesis

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13
Q

What does the cardiac cycle graph look like when you increase afterload, increase preload, or increase contractility?

A

Afterload = increased aortic pressure, decreased SV & EF, and increased ESV (right shifted, skinny, tall rectangle)

Preload = increased EDV, increased SV (curve expanded to the right)

Contractility = increased SV & EF, decreased ESV (curve expands upward and to the right)

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14
Q

What two diseases can cause a decrease in aortic elasticity?

A

Marfans & Syphilis

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15
Q

What can cause an S3 and S4?

A

S3: CHF or MR; increased filling pressures (normal in kids or pregz

S4: Aortic Stenosis, HTN; Atrial kick against a stiff ventricle

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16
Q

What are the waves in the Jugular Venous Pulse graph and what do they stand for?

A

A: The atrial kick at the end of contraction (S4 heard here followed by S1)
C: the Tricuspid back bulge of a full ventricle
X: Emptying of the RV taking pressure off of the atrium
V: Passive filling of the RA from the Vena Cavas (S2 heard towards the end)
Y: Passive emptying (not quite the kick yet) of the RA into the LV (S3 heard here)

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17
Q

When does the QRS occur in relation to the cardiac cycle?

A

When the Mitral Valve Closes

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18
Q

What causes normal splitting? Wide splitting? Fixed Splitting, Paradoxical Splitting?

A

Normal = splitting on inspiration due to increased venous return to the RA causing PV to close later than AV

Wide Splitting = RBBB or Pulmonic Stenosis; splitting heard regardless of breath

Fixed Splitting = ASD –> Left to Right shunt causing RV more filling and a delayed closure of the PV

Paradox: LBBB or Aortic Stenosis; Aortic Valve takes longer to close than Pulmonic Valve due to increased filling

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19
Q

What will inspiration and expiration do to heart murmurs?

Hand grip?

Valsalva?

Squatting?

A 
Inso = increase right sided sounds
Exp = increase left sided sounds

Hand grip = increase afterload (TPR) = increased MR, AR, VSD, MVP. (Will decrease AS and HCOM intensity)

Valsalva = decrease venous return (decrease preload and afterload) = increase MVP, or HCOM

Squatting = increase venous return = decrease MVP or HCOM

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20
Q

Describe the systolic murmurs: AS, MR, TR, MVP, VSD

A

AS: Crescendo-Decrescendo w/ Ejection Click. It will radiate to the carotids and may have parvus et tardus (weak pulses)

MR = Holosystolic, blowing. Heard at apex. Radiates to axilla

TR = Same as MR but heard at LLSB and increased with inspiration (IV drug users)

MVP = Late Systole w/ Mid systolic Click, heard at apex. Can be associated with infective endocarditis

VSD = heard in a newborn as a holosystolic, harsh murmur at LLSB

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21
Q

Describe the diastolic murmurs: AR, MS, TS, PDA

A

AR: Decresendo blowing murmur heard at RUSB. Causes a wide pulse pressure (low diastolic) with bounding pulses and head bobbing. Vasodilators will decrease the intensity

MS/TS: Has an opening snap that can sound like a split S2. LA»LV pressure during diastole

PDA: Machine murmur in a newborn, loudest at S2. Can be due to congenital rubella or prematurity

22
Q

What do I(f) channels do? What drugs slow them?

How do cardiac myocytes couple to each other?

A

I(f) channels are funny current channels responsible for the slow mixed Na/K inward current resulting in spontaneous depolarization of cardiac nodal cells
ACh/Adenosine will slow these channels and slow the rate of depolarization = decrease HR

Myocytes couple via gap junctions

23
Q

What creates the U wave on the EKG?

A

Hypokalemia or Bradycardia (U wave is the line after the T wave)

24
Q

What is the tx for torsades de pointes?

A

Magnesium Sulfate

25
Q

What bacterial infection can lead to a type 3 AV block?

A

Lyme Disease (borderella bordofori)

26
Q

What shape is the QRS in a type 3 block?

A

It is still narrow, indicating that the AV node is still running thangs

27
Q

What congenital abnormality is associated with a Delta wave?

A

A delta wave (early ventricular depolarization) is seen in WPW. This can lead to re-entry and possible SVTs

Tx w: Procainamide or Amiodarone

28
Q

What drugs can prolong the QT interval?

A

Macrolides, Chloroquine
Anti-psychotics (haloperidol and risperidone)
HIV P.I.s
Anti-arrythmics (quinidine, and class 3’s)

29
Q

What BP changes are recorded by the aortic arch and carotid arch?

A

Aortic arch (vagus) is triggered by elevations in BP only

Carotid arch (glossophar) is triggered by BOTH elevations and reductions in BP

30
Q

How do BaroR’s regulate BP?

A

Hypotension will decrease baroR firing –> increase in efferent sympathetic/decrease in parasympathetic firing leading to an increase in HR, contractility and BP

Hypertension (Carotid massage) will increase stretch and BaroR firing –> leading to a decrease in HR

31
Q

What changes in pressure do peripheral and central chemoRs sense?

A

Peripheral: (carotid and aortic bodies) are stimulated by low PO2 (<60mmhg) or high CO2 or low pH

Central: stimulated by low pH of high PCO2 only, NO oxygen sensing here

32
Q

What enzyme phosphorylates Myosin (so it can interact with actin and create SM contraction)?

What inhibits and activates this enzyme?

A

Myosin Light Chain Kinase is the enzyme

It is activated by calmodulin-Ca complex (blocked by Ca blockers like Nifedipine)

It is blocked by cAMP (stimulated by PGEs and Epinephrine via B2 R’s)

This shows how Nifedipine, PGEs, and Epi can lead to SM vasodilation

33
Q

What dephosphorylzes Myosin? (so it can not interact with actin thus creating vasodilation)

What inhibits and activates this enzyme?

A

Myosin Phosphatase is this enzyme

It is activated by high levels of cGMP (made from GTP via guanylyl cyclase)

Guanylyl Cyclase is activated by NO (Nitrates)
NO is made by L-arginine via iNOS (stimulated by LPS)

**Thus, Nitrates and Gram negative bacteria can lead to vasodilation

cGMP is broken down by cGMP phospodiesterases (which are inhibited by sildenafil)

**Thus, Viagra can indirectly cause more cGMP and thus more vasodilation

34
Q

What other cell type has an influence on SM contraction/dilation? By what mechanism?

A

Endothelial cells can release NO into SM cells via conversion of L-arginine to NO (via cNOS and high intracellular Ca)

cNOS is increased by bradykinin, ACh, a2 agonists, histamine, serotinin and shear stress

Thus all of these things can lead to vasodilation of SM cells

35
Q

What is the most important controlling mech in skin temp control?

A

sympathetic stimulation

36
Q

What are the differences between type A and B Aortic Dissection

What is the tx?

A

A = in the ascending or arch of the aorta; surgical

B = in the descending aorta; medical (B-blockers b/c this will decrease the pressure but also the steep slope of the rise in pressure

37
Q

In what way is HDV dependent on HBV?

A

It must be coated with HBV Ag in order to infect hepatocytes. Once it penetrates, it can replicate and stuff on its own

38
Q

Eukaryotes have multiple ORI

A

Prokaryotes only have 1

39
Q

What does the enzyme pyruvate carboxylase do? What process is it involved in and what regulates it?

A

Converts Pyruvate to OOA in one of the first steps of gluconeogenesis

It is upregulated by Acetyl CoA

40
Q

What is a red neuron? What does it look like histologically?

A

A red neuron is the result of an acute, irreversible neuronal injury where the nucleus is pyknotic, the neuron shrinks and the cytoplasm stains eosinophilic.

This can be due to ischemia, hypoxia, or toxicity or hypoglycemia

41
Q

What are the 3 signs of a VIPoma?

A

Watery Diarrhea, Hypokalemia, and Achlorhydria. These symptoms will persist even without food

It can be stopped by somatostatin

42
Q

What is thrombophlebitis of varying locations a sign of?

A

Pancreatic Adenocarcinoma

43
Q

What is Stewart-Treves Syndrome?

A

The development of a cutaneous angiosarcoma as a result of chronic lymphedema from a mastectomy.

Blood pools in the upper arm and is the risk factor

44
Q

What is the antidote for arsenic poisoning?

A

Dimercaprol

45
Q

How do you treat hypoglycemia in the field?

A

Intramuscular glucagon injection

46
Q

What are the three ways chromosomes can configure into Trisomy 21?

A
  1. 95% - Mieotic Nondisjunction from the moms side (increased age)
  2. 2-3% - Robertsonian Translocations
  3. Mosaicism
47
Q

What are the histological changes of urticaria? (Hives)

A

Superficial edema and lymphatic channel dilation. No epidermal changes are present

48
Q

What is a strawberry hemangioma?

A

Collection of unencapsulated aggregates of closely packed, thin walled capillaries.

They are present at birth and grow at first but than regress. They are benign

49
Q

What vitamin def resembles Friedreichs ataxia? What is the defect?

A

Vit E def.

Degeneration of spinocerebellar tracts and dorsal column of the spinal cord and peripheral nerves

50
Q

Where is the most common place for an aortic rupture after a car accident?

A

At the aortic isthmus (right after the subclavian artery branches off and the aorta starts to descend

51
Q

Which phase of metabolism do SLE inducing drugs (Hydralazine and Procainamide) use?

A

Phase 2 (acetylation)

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