Brainscape's Knowledge GenomeTM

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


See full index

Pathology > Path I Final Material > Flashcards

Path I Final Material Flashcards

1
Q

Hemostasis

A

the process of stopping blood loss

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

Coagulation

A

principle mechanism of hemostasis

fibrin forms a net and traps the formed elements in blood forming a blood clot

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

blood clot

A

mesh of protein filaments that trap bloods formed elements to forma a red, gelatinous mass

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

fibrin threads

A

threads that hold the blood cells together and they seal the wound to prevent losing blood

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

Clotting factors

A

present in the blood at all times in their inactive form

become activated upon injury through the intrinsic and extrinsic pathways

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

Where are clotting factors produced

A

in the liver

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

Which vitamin is required to produce clotting factors

A

vitamin k

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

CF I

A

fibrinogen

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

CF II

A

prothrombin

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

CF V

A

preaccelerin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

CF VII

A

proconvertin

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

CF VIII

A

antihemophilic factor

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

CF IX

A

christmas factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

CF X

A

stuart-prower factor

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

CF XII

A

Hageman Factor

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

CF XIII

A

fibrin-stabilizing factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What activates the extrinsic pathway for blood clotting?

A

damage to cells within blood vessels and outside the vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is released from injured cells to activate the extrinsic pathway for blood clotting?

A

Tissue factor aka tissue thromboplastin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does tissue factor activate?

A

proconvertin, which then activates stuart-prower factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is required to cause coagulation?

A

Fibrin which is the active form of fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What activates the intrinsic pathway for blood clotting?

A

exposure of collagen fibers of subendothelial cells of blood vessels to blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the only place the intrinsic pathway can be activated?

A

inside an injured blood vessel

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

What clotting factor do exposed collagen fibers activate?

A

Hageman factor which activates plasma thromboplastin antecedent (CF XI) which activates christmas factor which activates stuart-prower factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Both the extrinsic and intrinsic factors result in activation of which clotting factor?

A

CF X aka stuart prower factor

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

What does CF X activate?

A

the clotting cascade
prothrombin is activated to thrombin
thrombin activates fibrinogen to fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What ion is a necessary component of coagulation?

A

Ca++

patients with severe blood loss are given calcium chloride injections to help with blood clotting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Platelet plug

A

the result of platelet activation

mechanically blocks the damaged blood vessel

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

Where does platelet activation occur?

A

inside a damaged blood vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What causes platelet activation?

A

exposure of collagen fibers of subendothelial cells of blood vessels to blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

von Willebrand factor

A

circulating in the blood in its inactive form
becomes activated when it exposed to collagen fibers
attaches to platelets and forms a single layer of platelets over site of exposed collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What does von Willebrand factor do to platelets?

A

causes activation, allowing a second layer of platelets to attach

causes degranulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What do platelets release when they undergo degranulation?

A

ADP- promotes platelet activation
Thromboxane A2 (TxA2)- vasoconstriction
Growth factors- promote wound healing, fibroblast chemotaxis

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

Anticoagulation System

A

competes with coagulation

prevents excess or uncontrolled blood clotting

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

Three components of the anticoagulation system

A

hemodynamics
endothelial mediation
fibrinolytic system

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

hemodynamics

A

slow blood flow is important for coagulation otherwise activated CF’s will get washed out and a clot cannot be formed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Endothelial mediation

A

when a platelet plug is formed, surrounding uninjured endothelial cells release prostacyclin (PGI2) which prevents excess platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Fibrinolytic system

A

CF12 also activates tissue plasminogen activator which converts plasminogen to plasmin, resulting in degradation of activated CF’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Tissue Plasminogen activator

A

converts plasminogen to plasmin, resulting in degradation of acvtivated CF’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Petechiae

A

pinpoint sized hemorrhages

can be caused by scurvy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What nutritional deficiency causes petechiae?

A

Scurvy

vitamin C deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

purpura

A

“bruising” smaller than 2cm but larger than petechiae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Ecchymoses

A

bruises >2cm

can be caused by cushings or prolonged steroid use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Prolonged use of what drug can mimic the symptoms of Cushing’s disease?

A

steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What disease causes widespread ecchymoses

A

Cushing’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Cushing’s Syndrome

A

overproduction of corticosteroids from the adrenal cortex leads to brittle blood vessels, severe osteoporosis, obesity, diabetes, and high BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Thrombocytopenia

A

<140,000 platelets in the blood leads to an increased risk of hemorrhage
petechiae and purpura are typical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the normal amount of platelets found in blood?

A

250,000-300,000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Von Willebrand’s Disease

A

genetic, autosomal

Patients with this disease do not produce von Willebrand factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are some signs of von Willebrand’s disease

A

hemorrhagic gastroduodenitis- periodic leakage of blood from mucosa of the GI tract
menorrhagia-increased amount of blood lost during menstruation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

hemorrhagic gastroduodenitis

A

periodic leakage of blood from mucosa of the GI tract

leads to black stool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

menorrhagia

A

increased amount of blood lost during menstruation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

metrorrhagia

A

serious disorder, usually manifested by uterine cancer

bleeding between periods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

hemophilia

A

nonproduction of certain clotting factors
genetic disorder, x chromosome linked
small trauma can lead to severe blood loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Hemophilia A

A

nonproduction of CF VIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Hemophilia B

A

aka Christmas disease

nonproduction of CF IX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Hemoarthritis

A

common complication of hemophilia
trauma leads to blood in the joint spaces
iron from the heme destroys the joint cartilage
blood must be removed from the joint space to prevent degeration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Hemodynamic Disorders

A

disorders that arise from interruptions in normal blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Thrombosis

A

thrombus formation

platelet activation and aggregation without the threat of blood loss or vascular damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Thrombus

A

always originates from the vascular wall and always maintains point of contact with the vascular wall through von Wilebrand factor, only forms WITHIN the blood vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Characteristics of a thrombus in an artery

A

dense and strong

firm and small

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Characteristics of a thrombus in a vein

A

loose and weak

loose and large

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Lines of Zahn

A

a special type of thrombus characterized by visible and microscopic laminations produced by alternating layers of pale and dark

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what comprises the pale layer seen with lines of zahn?

A

platelets and fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what comprises the dark layer seen with lines of zahn?

A

red blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Where would you expect to find a thrombus with lines of zahn

A

the heart or aorta (arch region)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Endothelial Damage

A

predisposing factor to thrombosis

stretching of endothelial cells from the inner surface of blood vessel exposes collagen fibers and thrombus is formed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Hypertension

A

increase resistance of the vascular wall to the fluid

seriousl factor that promotes endothelial damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Hemodynamic stress

A

in the arteries

normal wear and tear results in arteriosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

what accelerates arteriosclerosis

A

hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Artherosclerosis

A

specific changes, such as plaque formation, in the arterial walls that leads to enothelial damage in the arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

iatrogenic thrombosis

A

rare, caused by medical care

i.e. iv lines or injections into veins damages the endothelia and results in thrombus formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Causes of reduced blood flow

A

cardiac damage
increased blood viscosity
physical inactivity
varicose veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Reduction of rate of blood flow leads to

A

disruption in axial blood flow, where platelets flow closer to the vessel wall leading to platelets being more easily activated due to their proximity to the vessel wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Cardiac Damage

A

reduces the heart’s pumping ability leading to a reduction in blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Myocardial Infarction

A

most common infarction
coagulative necrosis followed by replacement with connective tissue
dead heart tissue scars over with fibrotic tissue which is not contractile, leading to a decreased cardiac output near the fibrotic tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

mural thrombus

A

thrombi formed in the chambers of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Rheumatic Heart disease

A

mitral stenosis slows flood flow in the left atrium increasing the chance of thrombus formation which can kill the patient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What are two conditions that can lead to hyperviscosity of the blood

A

psoriatic arthritis

polycytemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Polycytemia

A

increased red blood cell count leads to increased friction against the vascular wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What can cause polycytemia

A

living at high altitudes, emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

erythemia

A

a type of leukemia
blood flows very slowly due to increased RBC count
patients could die due to thromboses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Normal red blood cell count

A

3-5 million/ cubic mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What does physical inactivity predispose a patient to?

A

thrombus in the venous system, especially the lower legs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is required to return blood to the heart from the lower extremities?

A

muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Varicose veins

A

tortuosity of the veins prevents closure of the valves as the walls of the veins separate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Turbulence

A

disruption of laminar blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

what causes turbulence in blood vessels?

A

narrowed portion of the lumen
expanded lumen, aneurysm
twists and turns (varicose veins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

hypercoagulation

A

increased ability of the blood to coagulate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

what causes hypercoagulation?

A 
extensive burns
certain kidney diseases 
heart failure
widespread metastatic tumor growth
birth control pills
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

sequela

A

the pathological consequences of an eent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Sequelae of thrombosis (6)

A 
resolution
organization
recanalization
propagation
infarction
Embolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Resolution

A

thrombus disappears due to high fibrinolytic function in the blood, therefore the least dangerous but also a high chance of developing another thrombus (transient ischemic attack)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Organization

A

phagocytic digestion of the thrombus 2-3 days after it forms, replaces by connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

recanalization

A

reorganization leads to formations of canals within the thrombus
endothelial cells line the canals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Propagation

A

enlargement of the thromus in areas open to clotting factors and their activation
usually occurs in veins where flow is slow and there are bifurcations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Infarction

A

the process in which an infarct is formed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

infarct

A

region of necrosis caused by oxygen deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

White infarct

A

develops in tissues that have 1 blood vessel supply ie the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

red infarct

A

when a tissue is supplies by more than one blood vessel ie lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Ischemic stroke

A

most common area for stroke

liquefactive necrosis with cavity formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

gliosis

A

the process of repairing the CNS via neuroglia in the brain

does not shrink which is a huge advantage for the brain

102
Q

what is the mechanism of infarction

A

thrombosis

103
Q

What is the most common factor that results in infarction

A

arthrosclerosis

104
Q

vasculitis

A

a factor leading to infarction
inflammation of the vessel wall due to autoimmune disease
all five components of inflammation are involved and leads to decreased lumen size and ischemia

105
Q

giant cell arteritis

A

in the superficial temporal artery
aka hortons disease
symptoms include headache, visibile tender arteries, fever, weakness, temporary loss of vision

106
Q

what often accompanies temporal arteritis

A

polymyalgia rheumatic- pain in the proximal regions of hip and shoulder muscles

107
Q

opthalmic arteritis

A

temporary loss of vision

permanent if left untreated

108
Q

paraesophageal hernia

A

stomach protrudes through diaphragm into thorax

diaphragmatic contractions occlude veins leading to infarction and gangrene

109
Q

Sheehan’s syndrome

A

aka postpartum syndrome
anterior pituitary hypertrophies during pregnancy and if hemorrhage occurs within the uterus, the body responds by vasoconstriction in the whole body leading to necrosis of the anterior pituitary which only has a venous blood supply

110
Q

Factors affecting infarction

A

tissue vulnerability
pattern of vascular supple
oxygen delivering capacity of the blood
rate of occlusion development

111
Q

anastomosis

A

union of two or more artery branches

112
Q

Embolism

A

sudden occlusion of blood vessels by an embolus

113
Q

embolus

A

an abnormal mass moving through the bloodstream

114
Q

thromboembolism

A

most common type of embolism

piece of thrombus breaks off

115
Q

Fat embolism

A

from long bone fractures

can cross capillaries and travel in reverse direction to the brain causing purpuric brain hemorrhage

116
Q

Air embolism

A

at least 300 mL

gas within the vessels would increase pressure and block fluid flow

117
Q

air lock

A

pathology in which air embolism blocks blood flow

118
Q

bends

A

aka caisson disease or divers disease
elevation changes and canges in concentration of nitrogen in blood due to pressure change
pt right side up so they can breathe out the gas

119
Q

Who named vitamins?

A

Kazimerz Funk- polish biochemist

december 1913

120
Q

Who discovered the first vitamin?

A

Elmer McCollum
discovered vitamin A
june 1913, Kansas city university

121
Q

Water soluble vitamins

A

B, C

122
Q

Fat soluble vitamins

A

ADEK

123
Q

Vitamin B1 is also known as

A

Thiamine

124
Q

Function of B1

A

maintains neural membranes and nerve conductions, especially in peripheral nerves
prevents development of cancer

125
Q

What is the most important source of B1?

A

the husks of grains

refined grains lose B1

126
Q

What demographic is more likely to be deficient in B1

A

Alcoholics
women in their first trimester
fast-growing teens

127
Q

Why are alcoholics likely to be B1 deficient?

A

alcohol competes with b1 in neural functions and in biochemical reaction

128
Q

Beriberi

A

vitamin B1 deficiency
severe nervous system disorder
discovered by Christiaan Eijkman

129
Q

Dry Beriberi

A

Vitamin B1 deficiency
effects the nervous system
characterized by non-specific peripheral polyneuropathy with myelin degeneration and disruption of all three neurological arcs

130
Q

which neruological arcs are disrupted with dry beriberi

A

sensory
motor
reflex

131
Q

maifestations of dry beriberi

A

wrist drop, foot drop, toe drop

paresthesia, numbness, loss of reflexes

132
Q

Wet beriberi

A

Vitamin B1 deficiency
heart
characterized by damage to the cardiovascular system

133
Q

manifestation of wet beriberi

A

enlargement of the heart with thinning of the muscle wall (flabby myocardium)
peripheral vasodilation
peripheral pitting edema
cardiac failure

134
Q

Wernicke encephalopathy

A

Vitamin B1 deficiency
Affects mamillary bodies in the brain leading to atrophy
characterized by psychological problems

135
Q

Psychological problems seen with Wernicke’s encephalopathy

A 
Global confusion
apathy
listlessness
disorientation
opthalmoplegia
136
Q

Opthalmoplegia

A

seen in Wernicke’s encephalopathy
paralysis of one or more eye muscles as a result of deep damage of the CNS resulting in irregular eye movements, not simultaneous
patient is close to death when this is seen

137
Q

Korsakoff’s psychosis

A 
Vitamin B1 deficiency 
three manifestations: 
anterograde amnesia- loss of memory of evens occurring after the cause of amnesia 
inability to acquire new inflammation
confabulation-excessive talking
138
Q

Vitamin B2

A

Riboflavin

139
Q

ariboflavinosis

A

riboflavin deficiency

does not effect nervous system

140
Q

What population usually experiences B2 deficiency

A

those with chronic debilitating disease, renal and oncologic disease

141
Q

Symptoms of ariboflavinosis

A

cheilosis
glossitis
superficial interstitial keratitis
dermatitis

142
Q

cheilosis

A

symptom of ariboflavinosis
non-inflammatory
cracks in the corner of the mouth, may lead to infection and become cheilitis (which is a secondary infection)

143
Q

Glossitis

A

symptom of ariboflavinosis

inflamed tongue, may lead to atrophy of the tissue and loss of taste

144
Q

Superficial interstitial keratitis

A

symptom of ariboflavinosis
hardening of the cornea
cornea is usually avascular, with B2 deficiency a capillary net forms around and penetrates into the cornea resulting in inflammation and corneal ulceration
ulceration is painful due to nociceptors
fibrosis and loss of vision with healing

145
Q

Dermatitis

A

inflammation seen in especially the nasolabial folds, behind the ears, and groin

146
Q

Vitamin B3

A

niacin, nicotinic acid, nicotinamide

used as medicine for its vasodilation ability, can be produced from tryptophan via normal gut flora

147
Q

B3 in plants

A

bound and cannot be absorbed when eaten

148
Q

B3 leads to

A

decreased production of low density lipoproteins (LDL’s) which leads to prevention of arteriorsclerosis

149
Q

Pellagra

A

vitamin B3 deficiency
The three D’s:
dermatitis- develops on skin exposed to the sun, casal’s necklace & glove-and-stocking lesions
diarrhea- atrophy of epithelial cells of interstitial mucosa with involvement of submucosal layer
dementia- degeneration of cortical neurons
Death

150
Q

Vitamin B6

A

pyridoxine
found in all foods
thermolabile- a small amount of heat will destroy it

151
Q

Which medications compete with B6 in biochemical reactions and can cause deficiency?

A

Ixoniazid- anti Tb, not used as frequently today
Estrogens- high production of hormone treatment
D-penicillamine- medicine used for the treatment of Wilson’s disease and systemic sclerosis

152
Q

Symptoms of B6 deficiency

A 
chelosis/chelitis
glossitis
peripheral polyneuropathy
convulsions (especially in infants and children)
increased sloughing of epithelial cells
153
Q

Nidus

A

organic core of urinary stones

in the case of B6 deficiency- a clump of epithelial cells from the increase in epithelial sloughing.

154
Q

Seborrheic dermatitis

A

seen with B6 deficiency
dandruff
scalp is scaly and greasy

155
Q

Vitamin B12

A

cyanocobalamin
aka extrinsic factor of castle
not found in plants, animal are the only food source
cannot be absorbed directly, requires assistance via proteins

156
Q

R-binder

A

secreted by the salivary glands
binds to B12 and carries it from the stomach to the duodenum
dissociates from B12 in the duodenum

157
Q

Intrinsic factor of castle

A

aka intrinsic factor
produced and secreted by the parietal cells of the stomach
binds to B12(aka extrinsic factor of castle) when it reaches the duodenum and then moves to the ileum
ileum has receptors which bring the intrinsic/extrinsic factor complex into the blood where they dissociate from each other

158
Q

Causes of B12 deficiency

A 
diet
autoimmune disorder (idiopathic)
159
Q

Autoimmune chronic gastritis

A

cause of B12 deficiency
immune system produces parietal canalicular antibodies which destroy parietal calls in the stomach resulting in a lack of intrinsic factor

160
Q

Blocking antibodies with B12 deficiency

A

autoimmune

bind to intrinsic factor, blocking the receptor for B12, and B12 cannot bind the intrinsic factor

161
Q

Binding antibodies with B12 deficiency

A

autoimmune

bind to receptors for intrinsic factor in the ileum

162
Q

B12 deficiency leads to:

A

pernicious anemia

demyelination

163
Q

Pernicious anemia

A

aka malignant anemia
a type of megaloblastic anemia
decreased RBC’s decreased hemoglobin in RBC’s or both
lack of B12 interferes with normal hematopoeisis

164
Q

Demyelination in B12 deficiency

A

irreversible myelin degeneration leading to a decreased rate of conduction
seen in posterior and lateral column tracts of the spinal cord, peripheral nerves, and DRG

165
Q

What are some results of demyelination in B12 deficiency

A

numbness/tingling in the hands/feet
ataxia(abnormal gate due to spinocerebellar tract involvement)
paraplegia- subacute combined degeneration of the spinal cord, affects PNS and sometimes CNS (megaloblastic madness)

166
Q

What is the correlation between severity of pernicious anemia and demyelination in B12 Deficiency?

A

No correlation

167
Q

What may exacerbate nervous system pathologies with B12 deficiency

A

folic acid supplementation

168
Q

What are two types of megaloblastic anemia?

A

Vitamin B12 deficient anemia- pernicious anemia

folic acid deficient anemia

169
Q

Megaloblastic Anemia

A

folic acid or B12 deficiency results in large blood cells

170
Q

Folic Acid’s role in hematopoeisis

A

donates carbon for DNA in red blood cells

171
Q

B12’s role in hematopoeisis

A

activates tetrahydrafolate

172
Q

Blastic cells

A

immature form of blood cells
normally only found in red bone marrow
will appear in circulation with megaloblastic anemia

173
Q

Normoblast

A

normal cells

174
Q

Megaloblast

A

mature, large cells

175
Q

Macrocytes

A

large cells

176
Q

Red Blood Cells in pernicious anemia

A

become macrocytes
too large to fit in the capillaries
cannot bend due to a rigid cell membrane, leading to decreased oxygen in the tissues

177
Q

Neutrophil behavior in megaloblastic anemia

A

become hypersegmented
nuclei have more than 5 lobes
normal is 2-5

178
Q

Pancytopenia

A

total decrease in the number of blood cells

179
Q

Anemia

A

decreased RBC’s

180
Q

Leukopenia

A

decreased WBC’s

181
Q

Thrombocytopenia

A

decreased platelets

182
Q

Does folic acid supplementation help in a B12 deficiency?

A

Yes by giving the patient carbon to make DNA, however the tetrahydrofolate can only be used once in the absence of B12

183
Q

Does B12 supplementation help in a Folic acid deficiency

A

No
if a patient is showing anemia due to folic acid defiency, there is no tetrahydrofolate, so adding a THF activator will not do anything

184
Q

Main differences between folic acid and B12 deficiency

A

folic acid deficiency causes cheilosis while B12 deficiency does not
B12 deficiency affects the nervous system and Folic acid does not ( with the exception of a developing fetus)

185
Q

Methotrexate

A

leukemia drug
inhibits reductase, thereby interfering with hematopoeisis
purpose is to inhibit cancer cell replication, leads to suppressed immune system

186
Q

Vitamin C

A

cannot be produced in the human body

found in many food sources

187
Q

Function of Vitamin C

A

hydroxylation of procollagen to hydroxyproline (hydroxylation increases tensile strength of connective tissue )
synthesis of collagen peptides
powerful antioxidant

188
Q

Vitamin C as an antioxidant

A

works with vitamin E, secures cell membranes from disruption with selenium
reduces oxidation of LDL’s

189
Q

Scurvy

A

vitamin C deficiency

190
Q

Symptoms of scurvy

A

bleeding diathesis
skeletal changes
delayed wound healing

191
Q

Bleeding diathesis

A

development of petchie and ecchymosis
bleeding gums, abnormal gum, development, tooth loss
subperiosteal and retrobulbar hematomas

192
Q

Subperiosteal hematomas

A

seen with scurvy
between bone and periosteum
leads to bleeding into joint space, iron destroys articular cartilage leading to hemarthrosis (secondary osteoarthritis)

193
Q

Retrobulbar hematomas

A

blood behind the eyeball

increased pressure pushes the eye forward leading to loss of vision

194
Q

Skeletal changes with scurvy

A

Bowed legs (in growing children)
tooth loss due to alveoli
protrusion of ribs and sternum (pigeon chest)

195
Q

Excessive Vitamin C

A

enhances the immune system however could result in relapse of a cold as the body eliminates vitamin c when there is an excess

196
Q

Vitamin A

A

discovered in 1913 by McCollum
has several forms
fat soluble, so must be eaten with fat to be absorbed

197
Q

Retinol

A

Form of Vitamin A
storage and transport form
90% is stored in the liver and is enough for a six month supply for the body

198
Q

Retinal

A

Form of Vitamin A

maintains normal vision in dim light

199
Q

Retinoic Acid

A

Form of Vitamin A

important in determining the life span of epithelial cells

200
Q

Carotinoids

A

natural precursors for retinal

201
Q

Retinoids

A

synthetic/artificial

teratogenic

202
Q

Function/Deficiency of Retinal

A

maintains normal vision in reduced light
important in the production of visual pigments in photoreceptors
deficiency results in night blindness aka chicken disease/blindness

203
Q

Visual pigment for rods

A

rhodopsin

204
Q

visual pigment for cones

A

iodopsin

205
Q

Retinoic acid functions

A

potentiation and differentiation of specialized epithelial cells, mainly mucous secreting cells
enhances immunity to infections, particularly in children

206
Q

Retinoic Acid Deficiency

A

Xeropthalmia, xerosis, sqpaumous metaplasia, follicular and papullar dermatosis, pulmonary infection, nidues formation

207
Q

Bitot’s Spots

A

due to retinoic acid deficiency

xerosis, sloughed epithelial cells of the conjunctiva form plaques close to the cornea

208
Q

Nidus

A

a urinary tract obstruction with an organic core

formed as a result of increased epithelial sloughing due to Retinoic acid deficiency

209
Q

Hypervitaminosis A

A

More common/dangerous with synthetic vitamin A use

210
Q

Acute Hypervitaminosis A

A

signs/symptoms similar to that of a brain tumor/intracranial pressure
headache, nausea/vomiting, papilledema (swelling of the optic disc)
must rule out high BP

211
Q

Chronic Hypervitaminosis A

A

Weight loss, nausea/vomiting, dry mucosa, bone/joint pain, hepatomegaly leading to liver fibrosis, DISH

212
Q

Vitamin E

A

alpha tocopherol
a collective name
4 tocopherols and 4 tocotrienols
antioxidants that neutralize free radicals
functions in cell membrane maintenance in concert with vitamin c and selenium

213
Q

Which types of cell membrane are most vulnerable to vitamin A deficiency

A

RBC’s

Neurons

214
Q

Vitamin A deficiency

A

nervous system pathology- axon degeneration in the posterior column of the spinal cord, loss of nerve cells in the DRG
myelin degeneration of sensory axons, degenerative changes in the spinocerebellar tract

215
Q

symptoms of spinocerebellar tract degeneration

A 
absent tendon reflexes
ataxia
dysarthria
loss of position and vibration sense
loss of pain sensation
216
Q

When does RBC pathology with vitamin E deficiency cause anemia?

A

in premature infants whose RBC’s are more susceptible to destruction

217
Q

Hypervitaminosis E

A

Decreased coagulative ability of blood due to interference with vitamin K, decreasing CF production

218
Q

Vitamin E inhibits

A

atheroma formation in atherosclerosis through reducing oxidation of LDL’s

219
Q

Vitamin K

A

coagulation of blood
produced by the gut flora
usually in any animal food products

220
Q

Vitamin K is important in producing which clotting factors

A

Prothrombin (CF 2)
Proconvertin (CF 7)
Christmas Factor (CF 9)
Stuart-Prower Factor (CF 10)

221
Q

Aside from clotting factors, vitamin K is also used to produce

A

Proteins

specifically osteocalcin

222
Q

Osteocalcin

A

produced with vitamin K

a hormone that promotes calcification of bones

223
Q

Vitamin K indirectly prevents

A

osteoporosis

224
Q

Vitamin K deficiency leads to

A

bleeding diathesis

225
Q

Hemorrhagic disease of newborns

A

could result in intracerebral hemorrhage (stroke)

226
Q

Why are newborns particularly susceptible to vitamin k deficiency

A

their gut flora is not yet established

227
Q

Symptoms of vitamin K deficiency

A 
intracranial hemorrhage
echimoses
melena
hematoma
hematurea
bleeding gums
228
Q

iron deficiency

A

hypochromic microcytic anemia

229
Q

iodone deficiency

A

hypothyroidism

goiter

230
Q

selenium

A

Kashan’s disease

myopathy, congestive cordiomyopathy

231
Q

copper

A

muscle weakness

hypopigmentation

232
Q

zinc

A 
acrodermatitis enteropathica
anoerxia, diarrhea
growth retardation
hypogonadism, infertility
impaired wound healing
impaired night vision
impaired immune function
depressed mental function
233
Q

PEM

A

protein energy malnutrition
range of clinical syndromes characterized by an inadequate dietary intake of proteins and calories to meet the body’s needs

234
Q

somatic protein compartment

A

skeletal muscle

reserve, only taken when needed

235
Q

Visceral protein compartment

A

predominantly in the liver

can determine of this compartment is used by checking the levels of albumin in the blood

236
Q

80% of normal weight is

A

malnourished

237
Q

60-80% of normal weight is

A

kwashiorkor

238
Q

<60% of normal weight is

A

marasmus

239
Q

Marasmus

A

lack of calories and protein
somatic compartment is used resulting in emaciated extremities
visceral protein compartment untouched (normal albumin levels)

240
Q

Symptoms of Marasmus

A 
emaciated extremities
head disproportionately larger
anemia
multivitamin dificiency
immunosuppressed
241
Q

Type I Hypersensitivity

A

anaphylactic type, allergy

242
Q

In Type I Hypersensitivity, there is a release of

A

vasoactive amines and other mediators from the mast cells or basophils and affecting vascular permeability and smooth muscles in various organs

243
Q

Which immoglobulin is released with a type I Hypersensitivity

A

IgE

244
Q

which cytokines are released with a type I Hypersensitivity

A

IL-4 and IL-5

245
Q

Type II Hypersensitivity

A

antibody dependent

mediated by antibodies directed against target antigens on the surface of cells or other tissue components

246
Q

Three subtypes of Type II Hypersensitivity

A

complement-dependent
Antibody-dependent cell mediated cytotoxicity
Antibody mediated cellular dysfunction

247
Q

Type III Hypersensitivity

A

immune complex mediated
hypersensitivity is mediated by deposition of antigen-antibody complexes, followed by complement activation and accumulation pf PMN’s

248
Q

Type IV Hypersensitivity

A

Cell-Mediated
Hypersensitivity reation, cell mediated response (no Ab/complements involved) with sensitized lymphocytes ultimately leads to cellular and tissue injury

249
Q

Delayed Type Hypersensitivity

A

Type IV

antigen activates CD4 T cells resulting in the release of cytokines and recruitment of macrophages

250
Q

T Cell Mediated cytotoxicity

A

Type IV
T8 cytotoxic cells
account for antiviral, antitumor and graft rejection

Pathology (4 decks)

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