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Pathophysiology Block 2 > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

Hemostasis

A

physiologic coagulation of blood in injured vessels with the purpose of preventing bleeding
‘blood stop’

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2
Q

Vascular constriction

A

injured vessels produce thromboxane A2 through release of arachidonic acid from cell membrane. Thromboxane A2 is a potent vasoconstrictor of smooth muscles of arteries

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3
Q

Formation of the platelet plug

A

platelet adheres to injured vessels with aid of exposed sub endothelial collagen, platelets recruit more platelets (by releasing arachidonic acid), plug is compacted by release of ADP, Ca2+, serotonin, and alpha-granule proteins. Fibrinogen also helps with platelet adhesion

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4
Q

Formation of the blood clot

A

Intrinsic pathway, extrinsic pathway

*See diagram

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5
Q

Fibrous organization

A

The clot becomes invaded by fibroblasts, which subsequently form CT all through or fibroblasts may dissolve it. Fibroblasts continue to complete organization of the clot into fibrous tissue within about 1 to 2 weeks

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6
Q

Petechiae

A

Small, purplish, hemorrhagic spots on the skin that appear in patients with platelet deficiencies (thrombocytopenia) and in many febrile illnesses

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7
Q

Purpura

A

Any rash in which blood cells leak into the skin or mucous membranes, usually at multiple sites. Purpuric rashes often are associated with disorders of coagulation or thrombosis

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8
Q

Vasculitis

A

Inflammation of a blood vessel

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9
Q

Hematoma

A

A swelling comprising a mass of extravasated blood (usually clotted) confined to an organ, tissue, or space and caused by a break in a blood vessel

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10
Q

Ecchymosis

A

Superficial bleeding under the skin or a mucous membrane; a bruise

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11
Q

Thrombosis

A

Formation/presence of a blood clot with the vascular system. Life saving during hemorrhage; life threatening any other time (clot can occlude a vessel and stop blood supply

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12
Q

Embolism/ thromboembolism

A

Sudden obstruction of a blood vessel by debris (blood clots, cholesterol plaques, masses of bacteria, cancer cells, amniotic fluid, fat from the marrow of broken bones, injected substances like air bubbles)

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13
Q

Infarction

A

Death of tissue from deprivation of its blood supply

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14
Q

Physical and chemical characteristics of platelets and their role in clotting

A

Platelets are not cells, they are broken off pieces of megakaryocytes, 2-4 microns in diameter. Lifespan: 10 days
SEE notes for how the clot…

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15
Q

Conversion of prothrombin to thrombin

A 
Factor Xa (activated factor X) catalyze Prothrombin --> Prothrombin
(Factor Xa is where the intrinsic and extrinsic pathways meet, ultimately both influencing the transformation of Prothrombin to thrombin)
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16
Q

Conversion of fibrinogen to fibrin

A

Thrombin catalyzes conversion of fibrinogen –> fibrin at site of vessel injury.
(Fibrin stabilizes and solidifies the aggregates into the final thrombus)

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17
Q

Development of a blood clot

A

Primary hemostasis: Platelet plug formation
1) Adhesion - VWF attracts platelets and adhere them to damaged areas to form initial platelet plug. Collagen receptors also aid with adhesion
2) Aggregation - Some platelets have platelet fibrinogen receptors that bind with fibrinogen to help them stick together which creates a stable clot
Secondary Hemostasis: Coagulation (Fibrin)
- Coagulation cascade of clotting factors (proteins) act in two ways: Extrinsic (more influential) and intrinsic. Both pathways meet at a “common” pathway where prothrombin is catalyzed to thrombin. Thrombin then catalyzes fibrinogen to fibrin, creating the fibrin clot.

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18
Q

Clot retraction

A

Contraction of blood clot

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19
Q

Lysis of blood clots

A

Fibrinolytic System:

  • Plasminogen catalyzed to plasmin, which physically breaks up the clot
  • Thrombin: both coagulative and anticoagulative. Anticoagulation - triggers thrombin-activated fibrinolysis inhibitor, which also cleaves the fibrin clot
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20
Q

Clotting cascade

Intrinsic, Extrinsic, and common pathways used in the initiation of clotting

A

See diagram…

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21
Q

Role of Vit. K in formation of blood clotting factors

A

Vitamin K is responsible for the formation of 4 important clotting factors in the Extrinsic, Intrinsic, and Common clotting pathways
-Extrinsic- Factor VII
- Intrinsic- Factor IX
- Common- Factor II (prothrombin, becomes thrombin), Factor X
Insufficiency of these results in serious bleeding
- IE “The Tea and Toast Diet” sometimes seen in the elderly population

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22
Q

Hemophilia

A

Bleeding disease where blood can’t clot b/c lack Factor VIII from mutation of X chromosome

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23
Q

Deep vein thrombosis

A

blood clot (thrombus) usually in leg, can cause swelling. Occur when don’t move (accident, airplane, bedrest), dangerous= can lead to pulmonary embolism

24
Q

Thrombocytopenia

A

low platelet count, easily bleed, skin has purple blotches

25
Q

Pulmonary embolism

A

blockage of pulmonary arteries from a traveling blood clot (thrombus); emergency!

26
Q

Disseminated intravascular coagulation

A

usually a complication from another disease; cascade of unnecessary formation of blood clots in small blood vessels, compromise blood flow and lead to organ damage. Normal clotting disrupted and severe bleeding can occur.

27
Q

Bleeding time

A
  • blood pressure cuff inflated on upper arm, two small cuts made below it
  • cuff deflated and cuts blotted every 30 seconds until bleeding stops
  • provides info about how quickly thrombi form in small vessels
28
Q

Platelet count

A
  • part of a CBC
  • provides info about whether pt’s platelets are within normal range
  • normal range ~150,00 - 300,000 / microliter
29
Q

Partial thromboplasm time (pTT)

A
  • clotting time in sec.
  • measures intrinsic pathway (Factors: 5 and 8-11)
  • good test for monitoring heparin therapy
30
Q

prothrombin time (PT)

A
  • clotting time in sec.
  • measures extrinsic pathway (factors 5,7,10)
  • good for montoring warfarin therapy
31
Q

D-dimer

A
  • detects presence of d-dimer (a fibrin degredation product)

- positive result indicates presence of thrombus (e.g. DVT or PE)

32
Q

Platelet function test

A
  • looks at
    - platelet ability to aggregate and create thrombus
    - strength of thrombus
    - responsiveness of platelets to chemotactic signals
  • useful for: diagnosing pathological thrombotic deficiencies (e.g. Van Willebrand’s, etc.)
33
Q

Mechanism which prevents excessive thrombosis (NONE)

A

TFPI
Antithrombin
Activated protein C
Plasmin

34
Q

Conditions that predispose a patient to developing pathologic thrombosis (NONE)

A

Genetic and acquired risk factors

  • Factor V leiden is a genetic mutation that can increase the risk of pathogenic clot formation by 5-7 fold (heterozygous) or 80 fold (homozygous). Still, the majority of people with this mutation will not develop a pathogenic clot.
  • However, when someone with this mutation has other acquired risks such as oral contraception, smoking, trauma, infection, surgery etc. their risk is increased significantly.
35
Q

Cortex

A

outer portion of kidney between capsule and medulla. Has projections called renal columns. Contains renal corpuscles and renal tubules, minus the loop of Henle (that’s in the medulla). EPO is formed here.

36
Q

Medulla

A

innermost section. Composed of “pyramids”. Contains structures responsible for salt and h2o balance in blood. Loop of Henle, vasa rectae, collecting tubule, etc.

37
Q

Pyramids

A

27 to 30 of these conical medullary structures make up the renal medulla. composed of interstitium and portions of loop of henle (and surrounding vasculature).

38
Q

Minor/major calyces

A

minor calyxes surround apex of renal pyramids. Urine flows through papilla at apex and into minor calyx. Two or three (or so) of these minor calyxes form a major calyx. Urine flows through these, into renal pelvis and to the ol’ ureters.

39
Q

Renal pelvis

A

funnel-like convergence at end of major calyxes Serves as passageway for urine to the ureters.

40
Q

Renal interstitium

A

is hypertonic, which draws h2o from thin, descending limb of loop of henle and collecting ducts(renal water reabsorption). efflux of urea from inner collecting duct creates the hypertonicity fyi/btw/yolo.

41
Q

Anatomy of a nephron

A

Afferent/efferent arterioles, Bowman’s capsule, glomerulus, juxtaglomerular apparatus (JGA), convuluted tubule - proximal/distal, ascending/descending loop of henle, collecting duct

42
Q

Afferent/Efferent arterioles

A

Afferent: Going in to the glomerulus. Arise from the cortical radial arteries supply to glomerulus
Efferent: Leaving the glomerulus. Leave the glomerulus to form the peritubular capillaries

43
Q

Bowman’s capsule

A

Encapsulates the glomerulus. Composed of a parietal layer and a visceral layer of stellate cells called podocytes. Bowman’s castle also forms the urinary space

44
Q

Glomerulus

A

One of the key components of the nephron. It is a bundle of specialized capillaries involved in the filtration of the blood to form urine

45
Q

JGA

A

It is the point where the thick ascending limb of the loop of hence come back in between the afferent and efferent arterioles of the glomerulus. Made up of the macula densa (specialized thick ascending limb epithelial cells), extra-glomerular mesangial cells (solid complex of cells to which the cells and basement membrane of the macula densa are attached), and granular cells (modified smooth muslcle cells in the terminal portion of the afferent arteriole that secrete renin.
JGA is vital for tubule-glomerular feedback and renin production and secretion

46
Q

Convuluted tubule (proximal/distal)

A

Long unbranching tube which is connected to the collecting duct by the collecting tubule
Proximal: in the cortex, it is the first segment that drains the bowman’s capsule, consists of coiled and then straight portions, 5/6 of sodium and water are reabsorbed in this portion
Distal: follows the macula densa of the JGA and connecting tot he collecting tube

47
Q

Ascending/Descending Loop of Henle

A

Descending: follow the proximal tubule, primarily in the inner medulla. Permeable to water but not solute
Ascending: after the hairpin loop of hence the tubule becomes the thin ascending limb then the thick ascending limb. Spans the medulla and into the cortex. Permeable to solute but not water

48
Q

Collecting duct

A

The final segment. Regulated by aldosterone (as well as ADH when you have low blood volume or decreased BP) Can open aquaporin’s to allow mass amounts of water reabsorption

49
Q

Functions of kidney

A

Excretory: Excretion
Non excretory: Regulation of salt content of the ECF, Regulation of the water balance of the body, Potassium regulation, Acid-base regulation, Metabolism of drugs/albumin/insulin, Synthesis of erythropoietin

50
Q

Excretion

A

Kidney excretes wastes from the body (urea, uric acid, creatinine, breakdown products of hemoglobin)

51
Q

Glomerular filtration

A

Urine formation (filtrate) begins at the glomerulus, with the bulk of the fluid arising from the glomerular capillaries and flowing into Bowman’s capsule.

52
Q

Tubular reabsorption and secretion

A

Almost all of the 180L of filtrate that is made each day must be reabsorbed (otherwise we’d pee alllllll day). Filtrate passes from Bowman’s capsule and into the tubules. As it moves along the tubules, the composition is altered via tubular reabsorption (removal of substances from the tube) or tubular secretion (adding of substances to the tube). This aids in maintaining substance and fluid balance in the body.
Tubular reabsorption - Moving substances from the lumen of the tubules back into epithelial tissue and eventually into the blood.
Tubular secretion - Moving substances from the epithelial tissues into the lumen of the tubules

53
Q

Assessment of glomerular filtration rate and its clinical relevance

A

The GFR is the amount of blood passing through the glomeruli each minute.
It is the best overall assessment of kidney function.
Estimated by determining clearance of particular substances.
This level can be assessed through a creatinine clearance test, which includes a urine and blood sample, then these results have to be calculated with the following factors to estimate true GFR: age, ethnicity, gender, height, weight.
Clinically relevant to see how well the kidney is filtering the blood. Can be helpful in dosing particular medications. Can help to assess rate of decline in kidney.

54
Q

TFPI

A

limits extension of blood clots

target: fact VIIa TF complex
effect: inhibition of extrinsic pathway

55
Q

Antithrombin

A

limits extension of blood clots

target: Haparin and endogenous glycoconjugates
effect: inhibition of factors VIIa, IXa, XIa, and thrombin

56
Q

Activated protein C

A

limits extension of blood clots

target: Factors V and VIII
effect: inhibition of formation of factor Xa and thrombin

57
Q

Plasmin

A

limits extension of blood clots

target: fibrin
effect: fibrinolysis

Pathophysiology Block 2 (7 decks)

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