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After midterm Flashcards

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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
causes of atery flow abnormalities
- cardiac damage - reduced pumping ability - rheumatic heart disease - MI - increased blood viscosity - polycythemia
26
Vein flow abnormalities
- physical inactivity(decreased muscular contraction required for flow) - varicose veins - reduction in rate of blood flow - turbulent blood flow
27
Varicose Veins
- 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
28
blood hypercoagulation
- hyperactivity of clotting factors - extensive burns - kidney disease - heart failure - cancer - infectious disease - birth control pills (#1)
29
birth control pills cause hypercoagulation
- decreased ability to prevent atherosclerosis - endocrine imbalance - hypercoagulation - difficulty becoming pregnant after stopping - increased risk cervical cancer 7-8x
30
sequela
pathological consequence of a particular event
31
5 parts of sequela thrombosis
``` 1- resolution 2-organization 3-recanalization 4-propagation 5-infarction 6-embolism ```
32
resolution (sequla thromosis)
- most benign - activation of fibrinolytic system - thrombus dissolved - TIA
33
TIA
- occur due to fibrynolytic effects - all stroke symptoms, lasts seconds - normal function after attack
34
blood loss to brain before damage
more than 15 min = brain damage
35
organization (sequela thrombosis)
- phagocytic digestion of thrombus | - usually 2-3 days post formation and development of CT where thrombus was on vascular wall
36
Recanalizaition (sequla thrombosis)
- dissolution of thrombus in peices, forming canals thru thrombus - endothelial tissue is formed around thrombi canals - deceased tissue not repaired
37
propagation
- enlargement of exisiting thrombus - usually within veins due to slow flow - can be extremely large - 90% in deep veins of leg
38
infarction (sequela thrombosis)
- process in which an infarct is formed | - major cause of death in US
39
infarct
-zone of necrosis due to oxygen deficiency
40
white infarct
- tissue supplied by only ONE blood supply | - heart
41
red infarct
- tissue supplied by more than 2 supply | - lung
42
arterial infarction
-damaged cells are replaced by CT
43
Ischemic stroke
- aka brain infarction - most common area for stroke - liquefactive necrosis with cavity formation - neuroglia are responsible for repairing lost tissue
44
Why does neuroglia repair damage of ischemic stroke
-bc if it were CT then it would shrink when healed, not good for brain tissue
45
Gliosis
-process of repair via neuroglia in brain
46
factors predisposing infarction
- ischemia - arterial thrombosis - vasospasm - vasculitis - venous infarction
47
ischemia
- CO intoxication | - directly affecting brain and heart
48
aterial thrombosis
-assoc w basilar or coronary a
49
vasospasm
-narrows lumens
50
vasculitis
- inflammation of vascular wall - dramatic narrowing of lumen - most common: temporal arteritis and polymylagia rheumatic
51
temporal arteritis
- 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
temporal arteritis aka
- giant cell arteritis | - hortons disease
53
polymayalgia rheumatic
- 50% patients with temporal arteritis present this - 15% with this present with temporal arteristis - dramatic muscle pain in neck, shoulder, pelvus - treated corticosteroids
54
Venous infarction
- less common - paraesphageal hernia - sheehan's syndrome
55
paraesophageal hernia
- 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
Sheehan's syndrome
- 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
factors affecting infarction
- tissue vulnerability to hypoxia - pattern of vascular supply - oxygen delievery capacity of blood - rate of development of occlusion
58
which tissues most vulerable to infarction
- brain - heart - liver is least
59
anastomoses
- 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
how does oxygen delivery affect infarction
-great oxygen capacity the less likely person will get ischemia
61
Embolism
-sudden occluison of blood vessel by abnormal mass moving within bloodstream
62
which embolism is most common
thromboembolism
63
venous thromboembolism
- --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
arterial thromboembolism
- thrombus commonly formed within left atrium or aortic arch | - breaks free and travels to organs with good blood supply
65
Fat embolism
- occurs with fat rich yellow bone marrow enters blood stream after fracture of long bone - small, numberous - lodge in small arterioles or capillaries
66
retraction of fat embolus
-emboi is compressed, allowing passage thru lung channel which pass by the capillary beds
67
skin or brain emboli
-causes petechial hemorrhanges within brain leading to death
68
alcoholism and emboli
-fat emboli can arise due to liver trauma in alcoholics
69
Kazimierz Funk
formulated concept of vitamins 1912
70
Elmer McCollum
discovery of first known vitamin | vitamin A 1913
71
Thiamine
- B1 - unrefined cereal, meat, legumes, peas, eggs - maintains nerve conduction thru building myelin
72
causes of thiamine deficiency
- diet of refined grain - alcohol (25% of def) - competes with B1 - periphreal nerve damage - polyvitamin deficiency
73
Beri Beri
-B1 thiamine deficiency
74
Dry BeriBeri
- symmetrical pheriphreal polyneuropathy- impairment of sense, motor, reflex arcs of periphreal nerves - myelin degeneration - wrist, foot, big toe drop - numbness - paresthesia
75
Wet BeriBeri
- cardiovascular syndrome - cardiac failure due to dramatic weakening of heart muscle - enlargement - flabymyocardium(thinning of wall) - peripheral vasodilation and edema
76
Wernicke- Korsakoff
``` Wernicke encephalopathy -global confusion -apathy -listlessness -disorientation -opthalmoplegia -nystagmus Korsakoff Psychosis -retrograde amnesia -inability to acquire new info -confabulation ```
77
opthalmoplegia
-improper movement of eyes, looking independant of each other
78
nystagmus
-rapid eye movement
79
confabulation
abnormal amount of talking
80
Riboflavin
- B2 | - dairy, meat, cereal, veggies, bacteria of GI tract
81
Ariboflavinosis
- B2 deficiency | - develops in ppl with serious disease; cancer, alchoholism, chronic infection (TB)
82
signs of symptoms of B2 deficiency
- cheilosis/cheilitis - glossitis - superficial interstitial keratitis - dermatitis(face, ears, genitals)
83
cheilosis/cheilitis
-drying and cracking of corners of mouth
84
superficial interstitial keratitis
development of capillaries in the cornea - inflammation - damaged/scar tissue - loss of transparency - ulceration of cornea - vision loss
85
Niacin in diet
B3 - grain, legumes, seed oils - production by body using tryptophan
86
Niacin function
- vasodilation | - decreased production of LDL
87
Niacin deficiency
- maize based diet | - tryptophan is bound and cannot be used to produce niacin
88
Pellagra
- niacin deficiency - dermatitis (cassals necklace) - diarrhea(atrophy of GI cells) - dementia - death
89
Pyrodoxine
- B6 - thermal labile substance, can be destroyed easily by heat - some medications compete leading to deficiency
90
Medications that compete with Pyrodoxine
- Izoniazid (anti TB) - Estrogens - D-penicillamine (treatment of wilsons disease
91
Estrogens and pyrodoxine
-estogens have hyperplastic activity, promotes replication of cells in endometrium, could lead to cancer
92
symptoms of pyrodoxine deficiency
- cheilosis/cheilitis - glossitis - peripheral polyneuropathy - convulsions - increased sloughing of epitheleal cells - nidus formatoin (urinary stones) - dandruff
93
Seborrheic dermatitis
- dandruff | - sign of pyrodoxine deficiency
94
Cobalamin aka
B12 or cyan
95
B12 absorbtion pathway
- salivatory gland - R-binder - bind B12 stomach - carry B12 to duodenum - split - B12 bound by intrinsic factor - intrinsic receptors of ilium - bloodstream
96
Causes of B12 deficiency
- low animal product intake - surgical removal of stomach - malnutrition/alcoholism - celiac disease - antacids - autoimmune
97
Autoimmune B12 deficiency
- 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
B12 function
-hematopoiesis

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