Brainscape's Knowledge GenomeTM

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


See full index

Mechanisms of Disease > Week 6 Cardiovascular > Flashcards

Week 6 Cardiovascular Flashcards

1
Q

What vascular diseases did we cover?

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

What diseases of the heart were covered?

A
  1. Myocardial Infarction
  2. Cardiac Hypertrophy
  3. Conduction Disorders
  4. Myocarditis
  5. Carcinoid Syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What Hematopathology diseases were covered?

A
  1. Anemia (Erythrocytes)
  2. Thombocytopenia (Platelets)
  3. Neutropenia (Leukocytes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Explain the causes of Hypertension.

A
  1. Essential Hypertension–> NOT explained by another disease
    - Sustained pressure increase
    Systolic over 140
    Diastolic over 90
    - Complex multigenic disorder
    Genetic predisposition
    Environmental factors
  2. Secondary Hypertension–> explained by another disease
    - Renal Dysfunction
    - Endocrine Dysfunction
    - Cardiovascular Dysfunction
    - Neurologic Dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do diuretics treat hypertension?

A

They force the kidney to NOT retain as much fluid; decreases blood volume, which decreases blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the blood pressure formula?

A

Blood pressure= Cardiac output + Peripheral resistance

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

What is peripheral resistance?

A

How much the blood vessels push on the blood itself
- Anything that affects constriction or dilation of blood vessels also affects peripheral resistance
- Ex: larger blood volume = more total pressure on the cardiovascular system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

2 types of Arteriosclerosis

A
  1. Hyaline
  2. Hyperplastic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe hyaline arteriosclerosis

A
  • Protein deposits
  • Narrow lumen of vessels
  • Associated with benign hypertension
  • Leak of plasma proteins past damaged epithelial cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe hyperplastic arteriosclerosis

A
  • Onion-skinning
    Smooth muscle and basement membrane- many layers
    PAS staining for basement membrane
  • Associated with severe hypertension
    Narrows lumen and causes hypertension to be worse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is arteriosclerosis?

A

Hardening of arteries
- happens over time
- damage to BVs causes sclerosis
- scar tissue forming around BVs b/c they are damaged by excessive pressure

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

What is Atherosclerosis?

A

Type of arteriosclerosis
- Characterized by formation of atheromas
Aka: atherosclerotic plaques
Lesion in tunica intima
Projects into lumen
- Core is lipids covered by fibrous cap
Body NOT handling lipids properly and they end up deposited in the walls of BVs

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

What is the difference b/t vulnerable atherosclerotic plaque and a stable plaque?

A
  1. Vulnerable
    - larger fibrous core with smaller/thinner fibrous cap
    - a lot of immune response
    - more vulnerable to breaking off and traveling through the blood
  2. Stable
    - Greater/thicker fibrous cap relative to lipid core = the more stable the plaque
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are cholesterol deposits?

A

Cholesterol clefts–> cholesterol crystalized out–> cholesterol crystals form and when tissue is processed the crystals are not stable and they get knocked out and you end up with cholesterol clefts in tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are foam cells?

A

Macrophages trying to digest lipids and failing to do so
- Macrophages with a foamy appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the 4 basic steps of atherosclerosis pathogenesis

A
  1. Endothelial cell dysfunction
  2. Formation of atherosclerosis plaque
  3. T cells-macrophage interaction
  4. Fracture of the plaque and thrombosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe atherosclerosis pathogenesis step 1: endothelial cell dysfunction

A
  • plaques initiate at sites where endothelium is intact
  • result from endothelial dysfunction–> stressors affecting endothelial function
  • Most important contributors are:
    1. Hemodynamic disturbances- where you are getting turbulence through lumen of BV
    2. Hypercholesterolemia- high cholesterol in lipoproteins can damage endothelial cells directly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Explain apoproteins and lipoproteins

A
  • liver makes apoproteins
  • apoproteins can bind to lipids
  • lipids are transported by apoproteins–> when lipids travel in complex with apoproteins, they are called lipoproteins
  • depending on relative amount of lipid and protein, you get different densities of lipoproteins
    Lipids are LESS dense then proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are common abnormalities of lipoproteins in Hypercholesterolemia?

A
  • increased LDL levels–> more lipid than protein
  • decreased HDL levels–> more protein than lipid
  • presence of abnormal lipoproteins–> may be modified in some way due to other disease processes affecting lipoproteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is chronic hyperlipidemia (in reference to hypercholesterolemia)

A
  • Increased LDL, Decreased HDL
  • Damage the intima by LDL accumulation
    –> macrophages attempt to remove
  • Directly affect endothelial cell function
    –> endothelial cells are sensitive to amount of lipid being transported in blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are oxidized LDLs and what do they do?

A
  • LDLs are oxidized by excess ROS
  • Directly damage endothelial cells by attaching to them
  • Ingested by macrophages through specific receptor (NOT LDL receptor)
  • Accumulates in phagocytes, which then appear foamy
  • Stimulate cytokine, growth factor, and chemokine secretion–> innate immune response to help the body cope with stress
    –> monocyte recruitment
  • Macrophages release ROS
    –> injure tissue and deplete NO–> removing a dilator, so more likely to have constriction (secondary hypertension b/c caused by hyperlipidemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is a fatty streak?

A

Area of fat accumulation in tunica intima with macrophages including foam cells
- NO fibrous cap yet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe atherosclerosis path. step 2: Fibrous Cap

A
  • Cytokines released during inflammatory rxn induce smooth muscle cell proliferation and ECM production
  • Smooth muscle cells migrate to endothelium
  • Fibrous cap forms
    –> Conversion of fatty streak into mature atheroma
  • ROS and cytokines continue to produce oxidized LDLs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the difference between fatty streak and mature atheroma?

A

fibrous cap in mature atheroma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe atherosclerosis path. step 3: Cell Migration

A
  • Normally leukocytes do not bind to endothelium
  • Dysfunctional endothelial cells express adhesion molecules
  • Bound leukocytes migrate into intima due to chemokines being produced by macrophages
  • T lymphocytes induce chronic inflammation
    –> release of inflammatory cytokines
  • Now you are going from macrophages trying to clean up some damage to a chronic inflammatory response in the atheroma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe atherosclerosis path. step 4: Thrombus Formation

A
  • Damaged endothelium provides focal point for platelet binding and activation
  • Accumulation of platelets produces blood clot
    –> inflammatory mediators contribute
  • Clot breaks free–> will travel and eventually block a smaller vessel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Pre-clinical phase of atherosclerosis progression

A

Normal artery–> fatty streak–> fibrofatty plaque–> advanced/vulnerable plaque

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Clinical phase of atherosclerosis progression
- Aneurysm and Rupture

A
  • Mural thrombosis
  • embolization
  • wall weakening
  • potential life-threatening hemorrhage
  • clot damages more of the wall–> damages tunica media and adventitia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Clinical phase of atherosclerosis progression
- Occlusion by Thrombus

A
  • Plaque rupture
  • plaque erosion
  • plaque hemorrhage
  • mural thrombosis
  • embolization
  • clot forming that completely occludes BV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Clinical phase of atherosclerosis progression
- Critical Stenosis

A
  • progressive plaque growth
  • NOT blood clot forming
  • plaque growing to a point that it blocks BV sufficiently enough to be noticed
  • lumen of BV too small for normal function b/c atheroma has gotten so large
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the consequences of atherosclerosis?

A
  • Obstruct blood flow
  • Rupture of plaque–> thrombosis
  • Weaken underlying tunica media
    –> aneurysm formation
    Coronary Artery Disease
  • Myocardial infarction responsible for 1/4 of deaths in US
  • If it happens in an artery assoc. with blood supply to the heart itself, you can get myocardial infarct (heart attack)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the clinical complications of atherosclerosis?

A

Location is critical
- Occlusion results in infarct
–>myocardial infarction- coronary arteries
–>cerebral infarction (stroke)- brain
–> peripheral vascular disease- smaller vessel in peripheral system
- Rupture results in hemorrhage
–>formation of thrombus
–> aortic aneurism- if happens in BV like the aorta, you can bleed out quickly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What can thrombosis (mobile plaque) cause?

A

Can produce distal occlusions and additional plaques
- can attach to the wall or get stuck somewhere and actually cause a new plaque to form in that area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Trace the blood flow through the heart.

A

From body–> vena cava–> Right atrium–> valve to Right ventricle–> pulmonary artery–> lungs–> pulmonary veins–> Left atrium–> valve to Left ventricle–> aorta–> rest of body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is ischemic heart disease?

A
  • Group of diseases
    - most common cause is atherosclerosis of coronary arteries
  • Caused by myocardial ischemia
    - lower perfusion than needed
    –>decreased blood flow
    –> increased need- heart beating faster than it is being perfused
36
Q

In ischemic heart disease, what does lack of blood flow affect?

A
  • Energy production- not getting enough nutrients to the area; not enough glucose/O2
  • Nutrient availability
  • Waste removal- waste accumulation in the area, which can cause tissue damage as well
37
Q

Name one type of ischemic heart disease.

A

Myocardial infarction
- necrotic damage to the myocardium

38
Q

Explain severe myocardial ischemia.

A

-Biochemical changes
–> increased lactate
–> decreased ATP availability
* Early intervention important*
- Small window of time before cells die and damage is irreversible (1st 30 minutes)
- Depends on ATP levels and accumulation of dangerous metabolites

39
Q

How does reperfusion impact myocardiocyte function and survival?

A

Reperfusion
- burst of ROS following resumption of O2-based energy production
- some cells can cope and will recover
- others will undergo necrotic cell death
- flow restoration takes time before leveling off; some cells keep dying even though they have blood flow (reperfusion injury)
- salvage = degree to which you stop reperfusion injury
- gain back function, but it will never be what it was= post-ischemic ventricular dysfunction

40
Q

Describe the stepwise process occurring in reperfusion injury.

A
  • O2 is taken away
  • cells switch to glycolysis
  • when O2 is added back, cells use O2 to make ATP again
  • lots of ROS produced
    - normally cells have antioxidants to cope with ROS, but when using glycolysis the cells have not been making antioxidants because they did not need to
  • still salvage about 60% of tissue with a loss of around 10% to reperfusion injury
41
Q

What proteins can be evaluated in the blood to assess the timing of a myocardial infarct?

A
  • Troponin I and CK-MB (myocardial creatine kinase) are very specific
  • Myoglobin is another one, but not as sensitive or specific to MI
  • This concept is useful for people without typical symptoms of MI (i.e. many women do not have chest pain)
42
Q

Describe the steps involved in necrotic cardiomyocytes releasing proteins.

A
  1. Onset of myocardial infarction
  2. Plasma membrane of necrotic myocytes becomes leaky
  3. Molecules leak out of the cell into circulation
  4. These molecules can be used as biochemical markers for diagnosis of MI
43
Q

What is cardiac hypertrophy?

A

Increase in size of the heart, specifically the ventricles, caused by the heart having to work harder for whatever reason

44
Q

What causes cardiac hypertrophy?

A

Increased workload
- due to increased BP (hypertension)
- due to increased volume to move
- due to damage to the wall (MI for example)
Cardiomyocytes add sarcomeres (myocardiocytes enlarged)
Myocardial infarct
* If you do not get increased vasculature to the area, hypertrophy can be caused by MI or hypertrophy can cause MI

45
Q

What are the 2 conduction disorders discussed?

A

Bradycardia
Tachycardia
- both Arrythmias= anything that affects normal HR

46
Q

What is the clinical definition of Bradycardia?

A

Decreased resting HR below 60 BPM

47
Q

What is the clinical definition of Tachycardia?

A

Increased resting HR above 100 BPM

48
Q

What are the 2 mechanisms of Bradycardia?

A
  1. Reduced SA node activity
    - contraction induced by slower pacemaker
    - multiple causes
    age
    drugs (Ca channel blockers, beta-blockers)
    sleep, fainting (vagus nerve hyperstimulation)
  2. Blocked conduction- signal from SA node needs to be transmitted throughout the heart, so anything that blocks movement through the heart will slow HR because the signal is not moving through properly
    - similar to causes above
    - also linked to certain diseases
49
Q

Describe what causes Tachycardia?

A

Classification
1. Wide QRS interval
- ventricular
- supraventricular with conductance issue
2. Narrow QRS
- usually supraventricular (AV node or above)
- include atrial fibrilation, atrial flutter, sinus tachycardia
- these are not as dangerous as wide QRS, but intervention is still necessary
Any can be related to tissue damage (infarct) in the heart

50
Q

What is an infection of the heart called?

A

Myocarditis
- inflammation due to infection of myocardium

51
Q

What is the most common cause of myocarditis in the US?

A

Viral infections
- enteroviruses like coxsackie virus A and B
- Non-infectious causes are autoimmune or drug hypersensitivity (drug allergy)

52
Q

What are the microscopic characteristics of myocarditis?

A
  • Edema (more space between cells)
  • Interstitial inflammatory infiltrates (immune cells)
  • Myocyte injury
53
Q

What is the difference between an infarct and an infection in the heart?

A
  • Type of inflammatory cells
  • Presence of edema in myocarditis (infection)
54
Q

What are 4 different responses you may see in a pathology slide of myocarditis?

A
  1. Lymphocytic
  2. Giant cell
  3. Hypersensitivity (Eosinophilic)
  4. Trypanosomes (worms/parasite)
    * Depending on what is causing the myocarditis, you might see different responses in the tissue
55
Q

What is carcinoid syndrome?

A

Cancer related disease
- cancer cells produce hormones that affect the heart tissue (NOT cancer of the heart)
- fibrotic lesion (excessive collagen deposition in certain areas
- thickened endocardium
* Affects heart function b/c you either have a smaller lumen with thickened endocardium or the fibrosis is causing less flexibility in something like a valve or the walls of the heart

56
Q

What is anemia?

A

Low blood RBCs
- can occur due to blood loss, hemolysis, or reduced erythropoiesis

57
Q

What are some things issues/diseases that can cause anemia?

A
  • Sickle cell- causes hemolytic anemia due to sickled RBCs rupturing and being lost
  • Iron deficiency- blood loss
  • Pernicious (aka megaloblastic)- reduce erythropoiesis
58
Q

What is the most common cause of iron deficiency anemia?

A

Bleeding
- menstruation
- GI bleeds- ruptured polyp or bleeding ulcur
- also associated with pregnancy- iron being used by fetus to make blood

59
Q

What are the body’s sources of iron?

A
  • Dietary iron is absorbed in the intestines
  • Iron is recycled from aged RBCs by macrophages in the spleen
    - macrophages extract iron from Hb to make it available to make more Hb and more RBCs
60
Q

What happens during reduced Hb synthesis of iron deficiency anemia?

A
  1. RBCs have lower Hb content- lower O2 carrying capacity of blood
  2. Lower O2 levels induce erythropoietin to be released by kidneys
  3. Stimulates bone marrow- increases platelets
  4. RBCs become microcytic
    - smaller/ varied size
    - hypochromic (less color, less Hb)
    - varied shape
61
Q

What are the clinical symptoms of iron deficiency anemia?

A
  • weakness
  • fatigue
  • malaise (feeling unwell)
62
Q

What causes pernicious anemia?

A

Lack of vit. B12

63
Q

Describe pernicious anemia.

A
  • Vit. B12 is required for thymidine synthesis- needed for DNA synthesis
  • Failure of DNA synthesis affects hematopoiesis
  • Megaloblastic (abnormally large blood cells and visible hemopoietic precursors) in peripheral blood
64
Q

Explain the pathogenesis of pernicious anemia.

A

Damage to fundic glands in stomach
- Vit. B12 absorption requires intrinsic factor
- Intrinsic factor produced by parietal cells in fundic glands in the stomach
Autoimmune attack on gastric mucosa
- Loss of parietal cells due to autoreactive T cells (primary affect)
- Antibodies that block (secondary affect)
binding to intrinsic factor
binding to receptor
proton pump (found in other cases of chronic gastritis

65
Q

What platelet disorders were discussed?

A

Thrombocytopenia
- Drug-associated immune thrombocytopenia
- Heparin-induced thrombocytopenia
- Thrombotic thrombocytopenic purpura

66
Q

What is thrombocytopenia?

A

Platelet levels below normal

67
Q

What does thrombocytopenia result from?

A

Decreased production
- Vit B12 deficiency–> affects hematopoiesis and decreases production of megakaryocytes that normally make platelets
- Hereditary
Decreased survival–> something destroying platelets
- Immune-mediated
- Thrombotic thrombocytopenic purpura (TTP)

68
Q

Explain drug-associated immune thrombocytopenia.

A
  • Immune-mediated destruction of platelets (often associated with certain drugs)
  • Quinine, quinidine, vancomycin
    bind platelet glycoproteins
    create antigens recognized by antibodies
    antibodies then mediate destruction of platelets
  • Heparin–> anti-coagulant
    type I- direct aggregation
    type II- venous/ arterial thrombosis
69
Q

Explain heparin- induced thrombocytopenia (HIT).

A

Aggregation produces thrombosis
- lower risk with low molecular weight heparin
Clots in large arteries
- vascular insufficiency
- deep vein thrombosis
- emboli can cause fatal lung disease

70
Q

Explain thrombotic thrombocytopenic purpura (TTP).

A

ADAMTS13 (a metalloprotease) hereditary deficiency causes abnormal vWF compelxes that adhere to platelets
- thrombotic clots in microcirculation
- accumulation of clots damages epithelium
Symptoms are episodic
- unknown factors contribute
- hemolytic anemia due to shear stress on RBCs
- purpura= small spots on skin due to clots in microcirculation

71
Q

What is leukopenia?

A

Lack of WBCs/ lack of granulocytes
Agranulocytosis is clinically relevant
- reduced neutrophil numbers that are clinically apparent
- more susceptible to bacterial/fungal infections b/c neutrophils fight those off as one of the 1st responders

72
Q

What are the 2 mechanisms of leukopenia?

A
  1. Ineffective/ inadequate granulopoiesis
  2. Increased removal/ destruction of granulocytes from the blood
73
Q

What is neutropenia?

A

Lack of neutrophils
- Absolute neutropenia–> no neutrophils made
- Agranulocytosis–> granulocyte deficiency
- Cyclic neutropenia–> rare genetic disorder that taught us about how neutrophils are produced

74
Q

What are the causes of impaired granulopoiesis?

A
  1. Suppression of hematopoietic stem cells
    - accompanied by anemia and thrombocytopenia
    - some things that cause anemia and thrombocytopenia will also cause lack of WBCs (ex: pernicious anemia)
  2. Defective precursors die in marrow
    - defective b/c no proper DNA synthesis
    - megaloblastic anemia
  3. Rare congenital disorders
    - inherited defects prevent proper differentiation
  4. Drug exposure (most common)
    - mechanism of impaired granulopoiesis
75
Q

What is cyclic neutropenia?

A
  • Rare disease that provides insight into mechanisms of neutrophil production and function
  • Lifetime history
    - every 3 weeks, for 3-5 days, neutrophil count drops near 0, then rebounds (very susceptible to infections during this time)
    - peripheral neutrophil/ monocyte counts oscillate in opposite phases of same 3 week cycle
76
Q

Explain the genetic basis and mutation involved in cyclic neutropenia.

A

Classic case is childhood onset
- potentially autosomal dominant
- rare instances of spontaneous mutation in adults
Mutation in Neutrophil elastase
- found in primary azurophilic granules of neutrophils and monocytes
- mutant is excessively inhibitory, which causes excessive troughs in production

77
Q

Describe neutrophil hematopoiesis.

A
  • Requires 2 weeks to mature
  • Survives peripherally for 12 hours
  • Normally, large storage pool of precursors in marrow
  • Neutrophil production normally occurs in waves
    - negative feedback inhibits neutrophil production= neutrophil elastase
    - source of oscillations in production
78
Q

Explain neutrophil oscillations.

A
  • Neutrophils in blood are normal
  • Time for maturation explains opposing cyclicity of the peripheral neutrophils and monocytes
  • Neutrophil elastase inhibits myeloblastic differentiation–> and inhibits it too much
  • Instead of restarting production when neutrophil levels are low, it drops completely to 0–> excessively inhibitory
79
Q

What role does cholesterol have in the development of atherosclerosis?

A
  • Atherosclerosis happens when the body is not handling lipids properly and the lipids end up deposited in the walls of blood vessels
  • Chronic hyperlipidemia - increased LDL, decreased HDL
    - damage to tunica intima by LDL accumulation that macrophages attempt to remove
    - directly affects endothelial cell function
    - endothelial cells are sensitive to amount of lipid transported in blood
    - endothelial cells weakened and they start letting things through, which starts the process of plaque/thrombus formation
80
Q

What is the relationship b/t hypertension, myocardial infarct, and arrhythmia?

A
  • Hypertension can cause MI or MI can cause hypertension if there is no increase in vasculature
  • Arrythmia is anything that affects normal HR
    - Bradycardia or tachycardia
    - arrythmia will be the result of hypertension or MI b/c blockage can slow HR (bradycardia) and tachycardia could be related to tissue damage developed in the heart (ex: infarct)
81
Q

Compare/ contrast the 2 types of arrhythmias.

A
  1. Bradycardia = <60 BPM resting HR
    - Reduced SA node activity due to age, drugs, sleep/fainting OR
    - Blocked conduction through the heart
  2. Tachycardia = >100 BPM resting HR
    - Wide QRS interval
    –> ventricular (very dangerous
    –> supraventricular with conductance issue
    - Narrow QRS interval
    –> usually supraventricular (AV node or above)
    –> includes atrial fibrillation, atrial flutter, sinus tachycardia (none as dangerous as wide QRS, but still needs intervention)
82
Q

Which layer(s) of the heart are involved in both myocarditis and cardiac hypertrophy?

A

Myocardium

83
Q

Compare/contrast pernicious anemia and iron-deficiency anemia.

A
  1. Iron-deficiency anemia
    - most commonly due to bleeding (menstruation, GI bleeds)
    - also assoc. with pregnancy
    - Iron sources: dietary iron absorbed in intestines, iron recycled from aged RBCs by macrophages in spleen
  2. Pernicious anemia
    - lack of Vit. B12–> required for thymidine synthesis–> needed for DNA synthesis
    - failure of DNA synthesis affects hematopoiesis
    - Megaloblastic= abnormally large cells and visible hematopoietic precursors in peripheral blood
    –> hypersegmented neutrophils
    - pathogenesis involves damage to fundic glands of stomach
84
Q

Why would anemia affect bone marrow?

A

Bone marrow hematopoiesis is affected
- w/out adequate iron, the marrow cannot produce enough hemoglobin for RBCs
- platelets are increased
- RBCs become microcytic= smaller varied size, hypochromic, varied shape

85
Q

If thrombocytopenia is a lack of platelets, why are these diseases characterized by thromboses?

A

Platelet aggregation produces thromboses
- antibody-heparin in heparin-induced thrombocytopenia

Mechanisms of Disease (10 decks)

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