Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Histology/Pathology > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

4 Stages of Normal Hemostasis

A
  • 1- endothelial injury —> transient vasoconstriction to dec blood flow to site
  • 2- primary homeostasis- exposed sub endothelial matrix —> platelet adhesion, activation and aggregation
  • 3- secondary homeostasis - tissue factor —> coagulation cascade —> forming fibrin clot
  • 4- fibrinolysis - counter-regaultion to dissolve clot/ restrict it to only site of injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

2 Types of Thrombi

A
  • White: mainly platelets forming platelet plaque; arteries

- Red: mainly RBCs forming thrombin; veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How are endothelial cells pro-thrombiotic?

A
  • Sub endothelial cells express von Willebrand factor once exposed (glue b/n thrombogenic vessel wall and Gp1b receptors of platelets) platelet adhesion
  • Activated endothelial cells make tissue factor —> extrinsic cascade AND secrete plasminogen activator inhibitor —> promotes thrombosis/dec fibrinolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How are endothelial cells anti-thrombiotic?

A
  • Endothelial prostacyclin (PG12) and NO —> vasodilation, muscle relax, inhibit platelet aggregation
  • Adenosine disphosphatase degrades ADP (ADP normally inc aggregation)
  • Heparin-like molecules which interact w/ antithrombin III to enhance it
  • Thrombomodulin - activates protein C which cleaves factors 5a and 8a
  • Tissue Factor Pathway Inhibitor - (TFPI) inactivates factor Xa and tissues factor 7a complex
  • tPA- activates plasminogen —> plasmin (major fibrinolytic agent)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

2 Types of Platelet Granules

A
  • Alpha granules - fibrinogen, vWF, clotting factors V and VIII, platelet factor 4, PDGF and p-selectin
  • Delta granules - ADP, ATP, Ca++, serotonin, epi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Primary Hemostasis

A
  • Adhesion —> shape change —> platelets secrete granules (platelet activation) —> activated platelets now secrete TxA2 (vasoconstrictor that stimulates platelet aggregation) and delta granules secrete ADP (mediator of aggregation)
  • Platelets (aggregates) held together by fibrinogen and GpIIb/IIIa receptors on platelets (cross links); GpIIb/IIIa inhibitors used as anticoagulants

Concomitant activation of thrombin stabilizes the platelet plug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Closure Time

A
  • Meas time required for platelet sample to plug a tube
  • ID low platelet function if prolonged but does not tell cause
  • Could be low platelet count, anti-platelet meds, reduction of proteins needed for platelet function, etc
  • Can screen for Von Willebrand Disease but not all platelet function disorders AND cannot predict risk of preoperative bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Secondary Hemostasis

A

**Coag Cascade

  • Series of amplifying enzymatic reactions that ends in thrombin (2A) activation —> fibrin (1a) formation
  • Each factor starts as a proenzyme (inactive form) then activated and can go on to act as enzyme in subsequent reactions
  • Each reaction requires activated enzyme, cofactor, proenzyme and phospholipid surface as scaffold
  • Also use Ca++ ions (from delta granules)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Extrinsic Path of Coag Cascade

A

Tissue injury —> tissue factor + 7a —> activates 10 —> activates prothrombin to thrombin (2) —> converts fibrinogen to fibrin (1a) AND activates factor 8 which helps in intrinsic path AND activates factor 13 which stabilizes fibrin polymers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

PT

A
  • Screens extrinsic path; add tissue factor and phospholipids to plasma; prolonged PT and normal aPTT suggest factor VII deficiency (affected by warfarin)
  • INR- international std ratio to compare PT b/n labs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Intrinsic Path of Coag Cascade

A

Factor 12 (Hageman Factor) is activated by HMWK collagen —> activates 11 —> activates 9 —> w/ help from factor 8 they activated factor 10 —> activates prothrombin to thrombin (2) —> converts fibrinogen to fibrin (1a) AND activates factor 13 which stabilizes fibrin polymers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

aPTT

A

Screens intrinsic path (12, 11, 9, 8); prolonged if deficiency in one of these factors; Von Will Disease; lupus anticoagulant disorder; heparin use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

4 Roles of Thrombin

A
  • Converts fibrinogen to fibrin
    • Activates factors 11, 5 and 8
    • Platelet activation through PARs
    • Pro-inflammatory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

2 Inhibitors of Coagulation Prod by Liver

A
  • Antithrombin III - inactivates thrombin (2) and inhibits 9a-12a (heparin potentiates antithrombin III)
  • Activated protein C - inhibits factors 5a and 8a; requires protein S co-factor and both require Vit K (so inhibited by warfarin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Fibrinolysis

A
  • Fibrinolytic cascase is mainly carried out by plasmin (breaks down fibrin —> D-dimers)
  • Plasminogen —> plasmin activated by tPA, urokinase-like plasminogen activator and streptokinase (bacterial product)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

von Willebrand Disease

A

deficiency in VWF - bleeding disorder

17
Q

Bernard Soulier Disease

A
  • deficiency in Gpb1 receptor; defective platelet adhesion to endo wall
18
Q

Glanzmann Thrombasthenia

A
  • deficiency in GpIIb/IIIa receptor; bleeding disorder b/c cannot aggregate
19
Q

4 Types of Hemorrhage

A

Hematoma- more of a solid lump; accumulation of blood enclosed in tissue or brain

  • Petechiae - tiny (1-2 mm); usually due to platelet dysfunction/deficiency or loss of vascular wall support
  • Purpura - medium (3-5 mm); similar causes to petechiae but also vasculitis (infection compromises vessel wall)
  • Ecchymoses- larger (> 1 cm); subcutaneous bruises that change from red/blue —> blue/green —> gold/brown as Hb broken down to hemosiderin
20
Q

Virchow’s Triad

A
  • 1- Endothelial Injury
    • Ulcerated atherosclerotic plaques, trauma, inflammation/vasculitis, stress of hypertension, toxic hypercholesterolemia, smoking toxins
    • Previous MI
  • 2- Abnormal Blood Flow
    • Turbulence from plaques
    • Stasis from a fib (decreased contractions), aneurisms, arterial dilations,
  • 3- Hypercoagulability
    • Genetic
      • Factor V Leiden mutation
      • Prothrombin gene mutation
      • Rare - deficiencies in antithrombin III, protein C or protein S
    • Acquired
      • Antiphospholipid Antibody Syndrome
      • Heparin Induced Thrombocytopenia-
    • Secondary hypercoagulable conditions: immobility, oral contraceptives, hormone replacement therapy, obesity, pregnancy, trauma, post-partum period
21
Q

Types of Shock

A
  • Cardiogenic - low cardiac output due to pump failure
  • Hypovolemic - low cardiac output due to loss of blood or plasma volume (usually must lose 20%)
  • Septic - systemic vasodilation, blood pooling, systemic immune rxn, microvascular thrombosis and end organ damage
  • Others - neurogenic (SC injury) or anaphylactic (systemic allergic reaction)
22
Q

Cardiogenic Shock

A
  • Causes: MI, cardiac tamponade, pulmonary embolus, ventricular arrhythmia
  • Treatment: Ionotropes to increase contractility or pressers; surgical bypass or percutaneous coronary intervention
23
Q

Hypovolemic Shock

A
  • Causes: burns, trauma, exsanguination, insanguination
  • Treatment: fluids and blood (if respond to this then confirms diagnosis of this type of shock); surgery to stop bleeding
24
Q

Septic Shock

A
  • Causes: bacterial or fungal infections

- Treatments: ANTIBIOTICS; fluids, insulin, corticosteroids for adrenal damage; treat DIC

25
Q

4 Main Events of Septic Shock

A
  • 1- Vascular
    • Vasodilation and inc permeability due to cytokines, dec perfusion (esp at micro vessels —> contributes to clot formation)
  • 2- Thrombotic
    • Complement activated and activates endothelial cells, microvascular thrombosis (DIC); endotoxins from bacteria —> pro-clot
    • DIC - clot formation and fibrinolysis at same time so both clots and bleeding in arterioles and capillaries deep in tissues
  • 3- Immunosuppressive
    • Hyper immune state then causes counter regulatory measures
  • 4- Metabolic
    • Insulin resistance, hyperglycemia, gluconeogenesis
    • Waterhouse-Friderichsen Syndrome- adrenal gland necrosis or hemorrhage into adrenal gland
26
Q

ARDS

A
  • ARDS (Adult Resp Distress Syndrome) - sometimes seen due to dec cardiac output, vascular permeability and endothelial damage in lungs —> pulmonary edema and acute damage (SEE HYALINE MEMBRANE FORMATION)
    • Edema damages alveoli so covered in membranous coating and no O2 gets to the area
27
Q

3 Stages of Shock

A
  • 1- Nonprogressive
    • Redistribution to conserve vital organs; so less flow to extremities (cold and pale) as well as inc in cardiac output to compensate
  • 2- Progressive
    • Lactic acidosis due to anaerobic metabolism; sign of hypoxia/anoxia (tissues not getting oxygen)
    • Lactic acidosis —> lower pH which blunts vasomotor response and worsens hypoxia and CO
  • 3- Irreversible
    • Organs start to shut down and stop functioning
    • Free radicals and NO accumulate —> dec contractility of heart
    • Ischemic bowel —> further bacteremia
    • Renal shut down as tubular necrosis starts
28
Q

SIRS

Sepsis

Severe Sepsis

Multi-Organ Failure

A
  • SIRS- systemic inflammatory response syndrome - non-specific response to infection or non-infectious inflammatory response; Must have 2+ of following:
    - Fever more than 38 deg C or less than 36 deg C
    - HR > 90 bpm
    - Resp rate > 20/min or PaCO2 < 32 mmHg
    - WBC > 12,000 or <4,000
  • Sepsis - SIRS + source of infection
  • Severe Sepsis - sepsis w/ organ dysfunction, hypotension or hypoperfusion
  • Multi-organ dysfunction syndrome (multi-organ failure) - septic shock w/ 2+ organs failing
29
Q

Active v Passive Congestion

A
  • Hypermia - active congestion - engorged w/ blood due to arterial dilation
  • Passive congestion - reduction in blood flowing out of the tissue due to back up
    • Ex) Nutmeg liver due to upstream L heart failure and pulmonary edema
    • Ex) Back up in spleen and liver “congestive hepatosplenomegaly
30
Q

5 Causes of Edema

A
  • 1- Inc hydrostatic pressure (too much pressure inside vessel forces fluid out)
    • Ex - deep vein thrombosis causing blockage
    • Results in transudate (protein poor)
  • 2- Dec plasma osmotic pressure
    • Dec in albumin in plasma —> can no longer keep fluid from leaking out
    • Dec b/c less synthesized by liver or protein lost in urine if nephrotic syndrome
    • Results in transudate (protein poor)
  • 3- Sodium Retention
    • Dec in renal blood flow causes kidney to retain Na+ and water via renin-angiotensin
  • 4- Inflammation (inc blood vessel permeability) - local or generalized
    • Results in exudate - protein rich pus
  • 5- Lymphatic Obstruction
    • Due to tumor, inflammation, surgery, radiation or scar; also parasitic infection
    • Also results in exudate
31
Q

Vegetations

A

non-bacterial but can become infected; can also be autoimmune or seen in cancer patients w/ inc hypercoagualbility

32
Q

4 Fates of Thrombus

A
  • 1- Dissolution - rapid shrinkage and dissolution due to fibrinolysis
  • 2- Propagation - further accumulation of fibrin and platelets
  • 3- Embolization - parts of clot break-off and dislodge —> end up in another part of vasculature
  • 4- Organization - recanalization; ingrowth of fibroblasts, smooth muscle cells, endothelial cells; form new lumen; flattens into a scar-like clump that narrows vessel
33
Q

5 Types of Emboli

A
  • Thromboemboli - most common; systemic thromboembolic most commonly travel from heart to legs or brain
  • Fat embolism - commonly from long bone fractures/trauma; clinically silent OR sudden dyspnea, tachypnea, tachycardia, restlessness, irritability, anemia, thrombocytopenia
  • Air embolism - air in IV infusion, scuba diving, sudden change in atmospheric pressure, chest wall injury, back surgery in prone position (need 100 mL for effect)
  • Amniotic fluid embolism - tears in placental membrane; squamous cells, lanuga hair, mucin or vernix cases fat travels from uterus —> lung (dyspnea, cyanosis, shock)
  • Paradoxical embolism - when clot travels from venous to arterial circulation thru patent foramen ovale, arterial septal defect, patent ductus arteriosus
34
Q

4 Determinants of Likelihood of Infarction

A
  • Organ’s vulnerability to hypoxia (ex- neurons very vulnerable- die after 4 min ischemia)
  • Rate of development of vascular occlusion (faster the occlusion occurs = less time to compensate)
  • Does organ have dual blood supply
  • Oxygen content of blood (may have co-morbidity hat dec O2 content - inc chance of infarct)
35
Q

2 Types of Infarction & Which Organs?

A
  • White- pale/anemic; normally if organ only has one source of blood flow (brain)
  • Red- hemorrhagic; if organ still gets blood from other sources (lung, liver, transverse colon, intestine)
36
Q

6 Types of Necrosis

A
  • Coagulative
    • Most common; architecture of dead tissue initially preserved; usual elicits acute inflammatory response (neutrophilic response peaks in 1-2 days then macrophages and fibroblasts)
  • Liquefactive
    • Dead tissue is digested and transformed into liquid mass (usually pus); lose architecture; common in brain
  • Gangrenous
    • Distinct form of coagulative; shrinkage and blackening; usually extremity or gallbladder; if infection on top of it then dry gangrene —> wet gangrene; if Chlostridium infection —> gas gangrene; treat w. surgical removal
  • Saponification
    • Fat necrosis; breakdown —> fatty acids which react w/ calcium to form chalky white soap-like material; appears bright white on histo image; usually in fat of extremities, pancreas (pancreatitis) and omentum
    • Can occur as a result of direct injury; usually accompanied by hemorrhage and destruction of surrounding its; may also get fat embolism (usually MVAs or pedestrian struck by motor vehicle)
  • Caseous
    • Associated w/ tuberculosis infection; granuloma look like cheese (necrotic centers and inflammatory borders)
  • Fibrnoid
    • In autoimmune reactions when antigen-antibody complexes build up in blood vessel walls
37
Q

Hemosiderin

A
  • By-product of iron metabolism; seen normally in certain cell types OR if iron overload
    • Normal circumstances- normal red cell breakdown; seen in mono-nuclear phagocytes of bone marrow, liver (Kipper cells) and spleen
    • Pathological - localized iron overload (seen in hemorrhage in form of bruises) OR systemic iron overload (ex- hereditary hemochromatosis)
  • Left behind by dead cells (not broken down by macrophages)
  • Gold/brown granular pigment (seen in images) OR can stain iron and it appears blue

Histology/Pathology (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions