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After midterm Flashcards

1
Q

thrombocytopenia

A
  • lack of platelets

- cause of various hemorrhange formation

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2
Q

normal thrombocyte number

A

300,000 mm

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3
Q

Von Willebrand disease

A
  • genetic disorder
  • cant produce von willbrand factor, no platelet aggregation
  • one or both parents have it
  • abdominal bleeding w pain
  • menorrhagia in women
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4
Q

hemorrhagic gastroduodenitis

A

-black stool

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5
Q

menorrhagia

A

-dramatic loss of blood during menstration

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6
Q

metrorrhagia

A
  • leakage of blood from uterus

- usually sign of uterine cancer

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7
Q

hemophilia A

A
  • classic

- non production of proconvertin XII

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8
Q

hemophilia B

A
  • christmas disease

- nonproduction of christmas factor

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9
Q

hemophliia

A
  • genetic
  • only in men
  • parents do not have
  • passed from mother
  • leakage of blood in the form of hematoma even with small injuries
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10
Q

hemoarthrosis

A
  • hematomas within the joints
  • esp knee
  • iron released from joint promotes DJD
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11
Q

Hemodynamic disorders

A
  • arise from interruption of normal blood flow

- #1 cause of death in US

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12
Q

Thombosis

A
  • formation of thrombus
  • only occurs in vessel
  • always originates from the vascular wall and always has a connection to vascular wall
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13
Q

blood clot

A

-can be formed inside or outside vessels

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14
Q

arterial system thrombus

A
  • fast flow

- dense, small

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15
Q

venous system thrombus

A
  • slow flow

- wide, large

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16
Q

Lines of Zahn

A
  • thrombi characterized by visible and microscopic laminations
  • pale layer platelets mixed w fibrin
  • dark layers RBCs
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17
Q

2 major locations lines of zahn

A

aorta
heat (mitral valve stenosis)
-usually post mortem

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18
Q

turbulent blood flow

A
  • any interruption of parallel laminar blood flow

- increases platelet contact with the vessel walls which can trigger activation

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19
Q

factors predisposing thrombsis

A
  • endothelial damage
    - exposure of membrane collagen to blow flow
    - hemodynamic stress
    - hypertension
    - atherosclerosis
    - iatrogenic thrombosis
  • flow abnormalities
  • blood hypercoagulation
  • birth control pills (#1)
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20
Q

hemodynamic stress

A

-normal wear and tear of blood vessels

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21
Q

hypertension as cause for thrombosis

A

increase the resistance within blood vessels increasing the hemodynamic stress rate

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22
Q

atherosclerosis as cause for thrombosis

A
  • formation of plaques within blood vessels, which causes increase resistance to or turbulent blood flow, can promote platelet activation
  • affects larger arteries
  • different than ateriosclerosis
  • 50% all death US
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23
Q

iatrogenic thrombosis

A
  • usually due to medical treatment from continuous intavenous injections into veins
  • leads to obliteration of vein
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24
Q

Artery flow abnormalities

A
  • reduction in rate of blood flow or stasis

- decreased rate causes disrupted axial blood flow, platelets to move to periphery of vessels an becomes activated (vWf)

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25
Q

causes of atery flow abnormalities

A
  • cardiac damage
    • reduced pumping ability
    • rheumatic heart disease
    • MI
  • increased blood viscosity
    • polycythemia
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26
Q

Vein flow abnormalities

A
  • physical inactivity(decreased muscular contraction required for flow)
  • varicose veins
  • reduction in rate of blood flow
  • turbulent blood flow
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27
Q

Varicose Veins

A
  • tortuosity, prevents closure of valves because the walls of the veins separate and the valves are not effective and flow goes without any restriction, increased hydrostatic pressure in lower leg veins
  • predisposing weakness of vein tone (congenital)
  • inactivity
  • vein compression(increase abdominal fat)
  • treatment is veins removed or burned
  • con be prone to burst
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28
Q

blood hypercoagulation

A
  • hyperactivity of clotting factors
  • extensive burns
  • kidney disease
  • heart failure
  • cancer
  • infectious disease
  • birth control pills (#1)
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29
Q

birth control pills cause hypercoagulation

A
  • decreased ability to prevent atherosclerosis
  • endocrine imbalance
  • hypercoagulation
  • difficulty becoming pregnant after stopping
  • increased risk cervical cancer 7-8x
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30
Q

sequela

A

pathological consequence of a particular event

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31
Q

5 parts of sequela thrombosis

A 
1- resolution
2-organization
3-recanalization
4-propagation
5-infarction
6-embolism
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32
Q

resolution (sequla thromosis)

A
  • most benign
  • activation of fibrinolytic system
  • thrombus dissolved
  • TIA
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33
Q

TIA

A
  • occur due to fibrynolytic effects
  • all stroke symptoms, lasts seconds
  • normal function after attack
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34
Q

blood loss to brain before damage

A

more than 15 min = brain damage

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35
Q

organization (sequela thrombosis)

A
  • phagocytic digestion of thrombus

- usually 2-3 days post formation and development of CT where thrombus was on vascular wall

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36
Q

Recanalizaition (sequla thrombosis)

A
  • dissolution of thrombus in peices, forming canals thru thrombus
  • endothelial tissue is formed around thrombi canals
  • deceased tissue not repaired
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37
Q

propagation

A
  • enlargement of exisiting thrombus
  • usually within veins due to slow flow
  • can be extremely large
  • 90% in deep veins of leg
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38
Q

infarction (sequela thrombosis)

A
  • process in which an infarct is formed

- major cause of death in US

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39
Q

infarct

A

-zone of necrosis due to oxygen deficiency

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40
Q

white infarct

A
  • tissue supplied by only ONE blood supply

- heart

41
Q

red infarct

A
  • tissue supplied by more than 2 supply

- lung

42
Q

arterial infarction

A

-damaged cells are replaced by CT

43
Q

Ischemic stroke

A
  • aka brain infarction
  • most common area for stroke
  • liquefactive necrosis with cavity formation
  • neuroglia are responsible for repairing lost tissue
44
Q

Why does neuroglia repair damage of ischemic stroke

A

-bc if it were CT then it would shrink when healed, not good for brain tissue

45
Q

Gliosis

A

-process of repair via neuroglia in brain

46
Q

factors predisposing infarction

A
  • ischemia
  • arterial thrombosis
  • vasospasm
  • vasculitis
  • venous infarction
47
Q

ischemia

A
  • CO intoxication

- directly affecting brain and heart

48
Q

aterial thrombosis

A

-assoc w basilar or coronary a

49
Q

vasospasm

A

-narrows lumens

50
Q

vasculitis

A
  • inflammation of vascular wall
  • dramatic narrowing of lumen
  • most common: temporal arteritis and polymylagia rheumatic
51
Q

temporal arteritis

A
  • chronic granulomatous inflammation of vascular wall of arteries
  • mainly temporal a
  • also opthalmic, leads to temp blindness, perm if not treated
  • and occurs in vertebral
  • corticosteriods
52
Q

temporal arteritis aka

A
  • giant cell arteritis

- hortons disease

53
Q

polymayalgia rheumatic

A
  • 50% patients with temporal arteritis present this
  • 15% with this present with temporal arteristis
  • dramatic muscle pain in neck, shoulder, pelvus
  • treated corticosteroids
54
Q

Venous infarction

A
  • less common
  • paraesphageal hernia
  • sheehan’s syndrome
55
Q

paraesophageal hernia

A
  • stomach herniates thru esophageal hiatus of diaphragm
  • diaphragm compresses and stops venous blood flow but not strong enough to completely block
  • build up of blood results stasis of arterial flow
  • gangrenous necrosis
56
Q

Sheehan’s syndrome

A
  • postpartum syndrome, occurs during delivery
  • anterior pituitary is supplied via venous system
  • hemorrhaging can occur during birth which causes systemic vasoconstriction
  • venous system cannot supply anterior pituitary and results in pituitary infarction
57
Q

factors affecting infarction

A
  • tissue vulnerability to hypoxia
  • pattern of vascular supply
  • oxygen delievery capacity of blood
  • rate of development of occlusion
58
Q

which tissues most vulerable to infarction

A
  • brain
  • heart
  • liver is least
59
Q

anastomoses

A
  • union of the branches of 2+ arteries supplying the same tissue or organ
  • physical activity increases them
  • thrombosis can be less severe because of this due to bloods ability to circumvent blockage
60
Q

how does oxygen delivery affect infarction

A

-great oxygen capacity the less likely person will get ischemia

61
Q

Embolism

A

-sudden occluison of blood vessel by abnormal mass moving within bloodstream

62
Q

which embolism is most common

A

thromboembolism

63
Q

venous thromboembolism

A
  • –deep leg veins- thrombus breaks free and travels to heart or lung
  • not dangerous but very painful
  • –GI tract- trombus breaks and goes to liver portal, detox issues, painless
64
Q

arterial thromboembolism

A
  • thrombus commonly formed within left atrium or aortic arch

- breaks free and travels to organs with good blood supply

65
Q

Fat embolism

A
  • occurs with fat rich yellow bone marrow enters blood stream after fracture of long bone
  • small, numberous
  • lodge in small arterioles or capillaries
66
Q

retraction of fat embolus

A

-emboi is compressed, allowing passage thru lung channel which pass by the capillary beds

67
Q

skin or brain emboli

A

-causes petechial hemorrhanges within brain leading to death

68
Q

alcoholism and emboli

A

-fat emboli can arise due to liver trauma in alcoholics

69
Q

Kazimierz Funk

A

formulated concept of vitamins 1912

70
Q

Elmer McCollum

A

discovery of first known vitamin

vitamin A 1913

71
Q

Thiamine

A
  • B1
  • unrefined cereal, meat, legumes, peas, eggs
  • maintains nerve conduction thru building myelin
72
Q

causes of thiamine deficiency

A
  • diet of refined grain
  • alcohol (25% of def)
    • competes with B1
      - periphreal nerve damage
    • polyvitamin deficiency
73
Q

Beri Beri

A

-B1 thiamine deficiency

74
Q

Dry BeriBeri

A
  • symmetrical pheriphreal polyneuropathy- impairment of sense, motor, reflex arcs of periphreal nerves
  • myelin degeneration
  • wrist, foot, big toe drop
  • numbness
  • paresthesia
75
Q

Wet BeriBeri

A
  • cardiovascular syndrome
  • cardiac failure due to dramatic weakening of heart muscle
  • enlargement
  • flabymyocardium(thinning of wall)
  • peripheral vasodilation and edema
76
Q

Wernicke- Korsakoff

A 
Wernicke encephalopathy
-global confusion
-apathy
-listlessness
-disorientation 
-opthalmoplegia
-nystagmus
Korsakoff Psychosis
-retrograde amnesia
-inability to acquire new info
-confabulation
77
Q

opthalmoplegia

A

-improper movement of eyes, looking independant of each other

78
Q

nystagmus

A

-rapid eye movement

79
Q

confabulation

A

abnormal amount of talking

80
Q

Riboflavin

A
  • B2

- dairy, meat, cereal, veggies, bacteria of GI tract

81
Q

Ariboflavinosis

A
  • B2 deficiency

- develops in ppl with serious disease; cancer, alchoholism, chronic infection (TB)

82
Q

signs of symptoms of B2 deficiency

A
  • cheilosis/cheilitis
  • glossitis
  • superficial interstitial keratitis
  • dermatitis(face, ears, genitals)
83
Q

cheilosis/cheilitis

A

-drying and cracking of corners of mouth

84
Q

superficial interstitial keratitis

A

development of capillaries in the cornea

  • inflammation
  • damaged/scar tissue
  • loss of transparency
  • ulceration of cornea
  • vision loss
85
Q

Niacin in diet

A

B3

  • grain, legumes, seed oils
  • production by body using tryptophan
86
Q

Niacin function

A
  • vasodilation

- decreased production of LDL

87
Q

Niacin deficiency

A
  • maize based diet

- tryptophan is bound and cannot be used to produce niacin

88
Q

Pellagra

A
  • niacin deficiency
  • dermatitis (cassals necklace)
  • diarrhea(atrophy of GI cells)
  • dementia
  • death
89
Q

Pyrodoxine

A
  • B6
  • thermal labile substance, can be destroyed easily by heat
  • some medications compete leading to deficiency
90
Q

Medications that compete with Pyrodoxine

A
  • Izoniazid (anti TB)
  • Estrogens
  • D-penicillamine (treatment of wilsons disease
91
Q

Estrogens and pyrodoxine

A

-estogens have hyperplastic activity, promotes replication of cells in endometrium, could lead to cancer

92
Q

symptoms of pyrodoxine deficiency

A
  • cheilosis/cheilitis
  • glossitis
  • peripheral polyneuropathy
  • convulsions
  • increased sloughing of epitheleal cells
  • nidus formatoin (urinary stones)
  • dandruff
93
Q

Seborrheic dermatitis

A
  • dandruff

- sign of pyrodoxine deficiency

94
Q

Cobalamin aka

A

B12 or cyan

95
Q

B12 absorbtion pathway

A
  • salivatory gland
  • R-binder
  • bind B12 stomach
  • carry B12 to duodenum
  • split
  • B12 bound by intrinsic factor
  • intrinsic receptors of ilium
  • bloodstream
96
Q

Causes of B12 deficiency

A
  • low animal product intake
  • surgical removal of stomach
  • malnutrition/alcoholism
  • celiac disease
  • antacids
  • autoimmune
97
Q

Autoimmune B12 deficiency

A
  • autoimmune chronic gastritis, immune system produces parietal canalicular antibodies which destroy parietal cells that produce intrinsic factor
  • blocking or binding antibodies- bind to intrinsic factor or bind to receptors
98
Q

B12 function

A

-hematopoiesis

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