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Blood Vessels > Everything except Pathology and Pharmacology > Flashcards

Everything except Pathology and Pharmacology Flashcards

0
Q

80yo man with 180/70 BP – cause of HTN?

A

isolated systolic hypertension
due to age-related decrease in compliance of the aorta and its proximal major branches (increased stiffness)

Isolated systolic HTN (ISH):

  • systolic BP elevated and considered hypertensive
  • diastolic BP is within normal range
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1
Q

What is the major proliferative stimuli for the cellular components of atherosclerotic plaques? Action?

A

Platelet-derived growth factor
released by locally adherent platelets, endothelial cells, and macrophages

PDGF promotes:
- migration of smooth muscle cells from the media into the intima
- increases smooth muscle cell proliferation
TGFbeta released by platelets also increases migration and induces interstitial collagen production by smooth muscle cells.

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2
Q

What is genomic imprinting and what is the mechanism? Describe the process.

A

offspring’s genes are expressed in parent-specific mannre
produced by DNA methylation

DNA methylation:

  • genes silenced by attachment of methyl groups to cytosine residues
  • methyl groups transferred from donors like S-adenosyl-methionine (SAM)
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3
Q

Which aortic arch gives rise to the ductus arteriosus? What other structures does it give rise to?

A

6th aortic arch

also gives rise to pulmonary arteries

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4
Q

How is a PDA closed? Maintained open?

A

closed with indomethacin

kept open with PGE2 infusions

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5
Q

What is the relationship between blood flow and vessel radius? Between resistance to blood flow and vessel radius?

A

Blood flow is directly proportional to the vessel radius to the 4th power
(r^4)

Resistance to blood flow is inversely proportional to the vessel radius to the 4th power (r^4)

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6
Q

What do the cardinal veins in the embryo give rise to?

A

the superior vena cava (SVC)

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7
Q

In early embryonic development, what are the three main groups of veins in the body? What do they become?

A

Vitelline - become the veins of the portal system
Umbilical - degenerate
Cardinal - form the veins of systemic circulation

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8
Q

What do the primitive atria and ventricle give rise to? The bulbus cordis? The primitive pulmonary vein? The right horn of sinus venosus?

A

Primitive atria - trabeculated part of both atria
Primitive ventricle - trabeculated part of both ventricles

Bulbus cordis - smooth part of both ventricles

Primitive pulmonary vein - smooth part of left atrium
Right horn of sinus venosus - smooth part of right atrium

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9
Q

What does the 1st aortic arch give rise to? 2nd? 3rd? 4th? 6th?

A

1st: MAXillary artery
2nd: Stapedial artery (regresses)
3rd: Common Carotid and proximal internal Carotid artery
4th: true aortic arch and subclavian arteries
6th: pulmonary arteries and ductus arteriosus

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10
Q

What does the 1st branchial/pharyngeal arch give rise to?

A

1st:

  • trigeminal nerve (CN V2 and V3)
  • muscles of mastication

2nd:

  • facial nerve (CN VII)
  • muscles of facial expression (Stapedius, Stylohyoid, etc.)

3rd:

  • glossopharyngeal nerve (CN IX)
  • stylopharyngeus

4th:

  • superior laryngeal branch of vagus (CN X)
  • pharyngeal constrictors

5th: obliterated

6th:

  • recurrent laryngeal branch of vagus (CN X)
  • intrinsic muscles of larynx
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11
Q

What does the thoracic duct drain and where does it empty?

A

entire left side of body and all regions inferior to umbilicus
empties into left subclavian vein

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12
Q

Follow the path of the IVC.

A
  • formed by the union of the left and right common iliac veins at the L4-L5 level
  • drains into the RA just above the level of the diaphragm at T8
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13
Q

Trace the path of the saphenous vein.

A
  • originates on medial side of the foot
  • courses anterior to medial malleolus
  • travels up medial aspect of leg and thigh
  • drains into femoral vein within region of the femoral triangle (inguinal ligament superiorly, sartorius muscle laterally, adductor longus muscle medially)
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14
Q

What are the stop codons? Initiation codon?

A

STOP codons: UAA, UAG, UGA

Initiation codon: AUG

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15
Q

What is the function of ApoE? What does absence result in?

A

mediates VLDL and chylomicron remnant uptake by the liver

Absence results in accumulation of chylomicrons and VLDL remnants form circulation, causing accumulation in serum (elevated cholesterol and TGs)

16
Q

What is the function of chylomicrons? Chylomicron remnants?

A

Deliver dietary TGs to peripheral tissue
secreted by intestinal epithelial cells.

Chylomicron remnants:
Deliver cholesterol to liver (mostly depleted of their TGs)

17
Q

What is the function of LDL? HDL? VLDL? VLDL is degraded into?

A

LDL: delivers hepatic cholesterol to peripheral tissue
HDL: reverse cholesterol transport from periphery to liver

VLDL: delivers hepatic TGs to peripheral tissue
degradation of VLDL forms IDL (delivers TGs and cholesterol to liver)

18
Q

What is the deficiency in Familial hypercholesterolemia? Inheritance?

A

absent or defective LDL receptors

Autosomal dominant

19
Q

What is the first step in the development of atherosclerosis? What cells are involved?

A

Pathogenesis of atherosclerosis begins with endothelial cell injury.

Endothelial cell dysfunction:

  • results in increased permeability (allows LDL cholesterol into intima)
  • monocyte/lymphocyte adhesion and migration into intima
  • platelet adhesion/activation
20
Q

What are bicarbonate and PaCO2 levels in metabolic acidosis? Respiratory acidosis?

A

metabolic acidosis:
bicarb is low
PaCO2 is low (immediate respiratory compesation)

respiratory acidosis:
bicarb is high or normal (delayed metabolic compensation by kidneys)
PaCO2 is high

21
Q

Given hydrostatic and oncotic pressures in the glomerular capillaries and in Bowman’s capsule, how would you calculate net filtration?

A

Net filtration pressure =
(Hydrostatic pressure gradient between capillaries and interstitium) - (Oncotic pressure gradient between capillaries and interstitium)

or (HPgc- HPbc) - (OPgc - OPbc)

22
Q

Which has lower oxygen content: pulmonary artery or coronary sinus?

A

coronary sinus (drainage of coronary venous blood)

myocardial O2 extraction exceeds that of any other tissue or organ in the body!!

23
Q

What are the mechanisms that exist to increase cardiac perfusion?

A

main mechanism: hypoxia and adenosine accumulation leads to coronary vasodilation and decreased vascular resistance to increase coronary blood flow

24
Q

Are COX enzymes constitutively expressed or induced during inflammation?

A

COX-1 is a constitutively expressed enzyme.

COX-2 is an inducible enzyme that is normally undetectable in most tissues, EXCEPT in cases where inflammatory cells are activated.

25
Q

What factor determines risk of acute plaque change producing acute coronary syndrome?

A

most related to plaque stability

plaque stability depends significantly on mechanical strength of fibrous cap (fibrosis mediated by smooth muscle cells)
inflammatory macrophages in the intima may secrete metalloproteinases, which degrade collagen and reduce plaque stability!!

26
Q

What does frothy, foamy urine indicate?

A

may be caused by proteinuria or bile salts in the urine

27
Q

What cofactor is required for the conversion of homocysteine to methionine?
What cofactor is required for the conversion of homocysteine to cysteine?

A

vitamin B12 (cobalamin)

vitamin B6 (pyridoxal phosphate)

28
Q

Describe the reaction that takes Homocysteine to Methionine.

A

B12-dependent

methylated tetrahydrofolate (CH3-THF) transfers its methyl group to homocysteine to produce methionine

29
Q

Describe the production of homocysteine from methionine.

A
  • Methionine gets an adenosyl put on it from ATP to form S-adenosyl methionine (SAM)
  • Methyl transferase takes a methyl off of SAM to form S-adenosyl homocysteine (SAH)
  • Adenosyl group is taken off of SAH to form homocysteine

(Remember, methionine is homocysteine + a methyl group)

30
Q

In atherlosclerosis, intimal thickening and collagen deposition seen. What cells are responsible for this intimal response?

A

predominantly mediated by reactive smooth muscle cells
(migrated form the media across the internal elastic lamina into the intima)
SMC proliferation and collagen synthesis produces a neointima, resulting in reactive intimal hyperplasia.

Macrophages can also contribute to the process of intimal thickening.

31
Q

What is reperfusion injury?

A

resumption of blood flow causes accelerated apoptosis or necrosis

caused by:

1) oxygen free radical generation by parenchymal cells, endothelial cells, and leukocytes
2) severe, irreversible mitochondria damage
3) inflammation (neutrophil attraction and activation of complement)

Blood Vessels (3 decks)

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