After midterm Flashcards
thrombocytopenia
- lack of platelets
- cause of various hemorrhange formation
normal thrombocyte number
300,000 mm
Von Willebrand disease
- genetic disorder
- cant produce von willbrand factor, no platelet aggregation
- one or both parents have it
- abdominal bleeding w pain
- menorrhagia in women
hemorrhagic gastroduodenitis
-black stool
menorrhagia
-dramatic loss of blood during menstration
metrorrhagia
- leakage of blood from uterus
- usually sign of uterine cancer
hemophilia A
- classic
- non production of proconvertin XII
hemophilia B
- christmas disease
- nonproduction of christmas factor
hemophliia
- genetic
- only in men
- parents do not have
- passed from mother
- leakage of blood in the form of hematoma even with small injuries
hemoarthrosis
- hematomas within the joints
- esp knee
- iron released from joint promotes DJD
Hemodynamic disorders
- arise from interruption of normal blood flow
- #1 cause of death in US
Thombosis
- formation of thrombus
- only occurs in vessel
- always originates from the vascular wall and always has a connection to vascular wall
blood clot
-can be formed inside or outside vessels
arterial system thrombus
- fast flow
- dense, small
venous system thrombus
- slow flow
- wide, large
Lines of Zahn
- thrombi characterized by visible and microscopic laminations
- pale layer platelets mixed w fibrin
- dark layers RBCs
2 major locations lines of zahn
aorta
heat (mitral valve stenosis)
-usually post mortem
turbulent blood flow
- any interruption of parallel laminar blood flow
- increases platelet contact with the vessel walls which can trigger activation
factors predisposing thrombsis
- endothelial damage
- exposure of membrane collagen to blow flow
- hemodynamic stress
- hypertension
- atherosclerosis
- iatrogenic thrombosis - flow abnormalities
- blood hypercoagulation
- birth control pills (#1)
hemodynamic stress
-normal wear and tear of blood vessels
hypertension as cause for thrombosis
increase the resistance within blood vessels increasing the hemodynamic stress rate
atherosclerosis as cause for thrombosis
- 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
iatrogenic thrombosis
- usually due to medical treatment from continuous intavenous injections into veins
- leads to obliteration of vein
Artery flow abnormalities
- 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)
causes of atery flow abnormalities
- cardiac damage
- reduced pumping ability
- rheumatic heart disease
- MI
- increased blood viscosity
- polycythemia
Vein flow abnormalities
- physical inactivity(decreased muscular contraction required for flow)
- varicose veins
- reduction in rate of blood flow
- turbulent blood flow
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
blood hypercoagulation
- hyperactivity of clotting factors
- extensive burns
- kidney disease
- heart failure
- cancer
- infectious disease
- birth control pills (#1)
birth control pills cause hypercoagulation
- decreased ability to prevent atherosclerosis
- endocrine imbalance
- hypercoagulation
- difficulty becoming pregnant after stopping
- increased risk cervical cancer 7-8x
sequela
pathological consequence of a particular event
5 parts of sequela thrombosis
1- resolution 2-organization 3-recanalization 4-propagation 5-infarction 6-embolism
resolution (sequla thromosis)
- most benign
- activation of fibrinolytic system
- thrombus dissolved
- TIA
TIA
- occur due to fibrynolytic effects
- all stroke symptoms, lasts seconds
- normal function after attack
blood loss to brain before damage
more than 15 min = brain damage
organization (sequela thrombosis)
- phagocytic digestion of thrombus
- usually 2-3 days post formation and development of CT where thrombus was on vascular wall
Recanalizaition (sequla thrombosis)
- dissolution of thrombus in peices, forming canals thru thrombus
- endothelial tissue is formed around thrombi canals
- deceased tissue not repaired
propagation
- enlargement of exisiting thrombus
- usually within veins due to slow flow
- can be extremely large
- 90% in deep veins of leg
infarction (sequela thrombosis)
- process in which an infarct is formed
- major cause of death in US
infarct
-zone of necrosis due to oxygen deficiency
white infarct
- tissue supplied by only ONE blood supply
- heart
red infarct
- tissue supplied by more than 2 supply
- lung
arterial infarction
-damaged cells are replaced by CT
Ischemic stroke
- aka brain infarction
- most common area for stroke
- liquefactive necrosis with cavity formation
- neuroglia are responsible for repairing lost tissue
Why does neuroglia repair damage of ischemic stroke
-bc if it were CT then it would shrink when healed, not good for brain tissue
Gliosis
-process of repair via neuroglia in brain
factors predisposing infarction
- ischemia
- arterial thrombosis
- vasospasm
- vasculitis
- venous infarction
ischemia
- CO intoxication
- directly affecting brain and heart
aterial thrombosis
-assoc w basilar or coronary a
vasospasm
-narrows lumens
vasculitis
- inflammation of vascular wall
- dramatic narrowing of lumen
- most common: temporal arteritis and polymylagia rheumatic
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
temporal arteritis aka
- giant cell arteritis
- hortons disease
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
Venous infarction
- less common
- paraesphageal hernia
- sheehan’s syndrome
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
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
factors affecting infarction
- tissue vulnerability to hypoxia
- pattern of vascular supply
- oxygen delievery capacity of blood
- rate of development of occlusion
which tissues most vulerable to infarction
- brain
- heart
- liver is least
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
how does oxygen delivery affect infarction
-great oxygen capacity the less likely person will get ischemia
Embolism
-sudden occluison of blood vessel by abnormal mass moving within bloodstream
which embolism is most common
thromboembolism
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
arterial thromboembolism
- thrombus commonly formed within left atrium or aortic arch
- breaks free and travels to organs with good blood supply
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
retraction of fat embolus
-emboi is compressed, allowing passage thru lung channel which pass by the capillary beds
skin or brain emboli
-causes petechial hemorrhanges within brain leading to death
alcoholism and emboli
-fat emboli can arise due to liver trauma in alcoholics
Kazimierz Funk
formulated concept of vitamins 1912
Elmer McCollum
discovery of first known vitamin
vitamin A 1913
Thiamine
- B1
- unrefined cereal, meat, legumes, peas, eggs
- maintains nerve conduction thru building myelin
causes of thiamine deficiency
- diet of refined grain
- alcohol (25% of def)
- competes with B1
- periphreal nerve damage - polyvitamin deficiency
- competes with B1
Beri Beri
-B1 thiamine deficiency
Dry BeriBeri
- symmetrical pheriphreal polyneuropathy- impairment of sense, motor, reflex arcs of periphreal nerves
- myelin degeneration
- wrist, foot, big toe drop
- numbness
- paresthesia
Wet BeriBeri
- cardiovascular syndrome
- cardiac failure due to dramatic weakening of heart muscle
- enlargement
- flabymyocardium(thinning of wall)
- peripheral vasodilation and edema
Wernicke- Korsakoff
Wernicke encephalopathy -global confusion -apathy -listlessness -disorientation -opthalmoplegia -nystagmus Korsakoff Psychosis -retrograde amnesia -inability to acquire new info -confabulation
opthalmoplegia
-improper movement of eyes, looking independant of each other
nystagmus
-rapid eye movement
confabulation
abnormal amount of talking
Riboflavin
- B2
- dairy, meat, cereal, veggies, bacteria of GI tract
Ariboflavinosis
- B2 deficiency
- develops in ppl with serious disease; cancer, alchoholism, chronic infection (TB)
signs of symptoms of B2 deficiency
- cheilosis/cheilitis
- glossitis
- superficial interstitial keratitis
- dermatitis(face, ears, genitals)
cheilosis/cheilitis
-drying and cracking of corners of mouth
superficial interstitial keratitis
development of capillaries in the cornea
- inflammation
- damaged/scar tissue
- loss of transparency
- ulceration of cornea
- vision loss
Niacin in diet
B3
- grain, legumes, seed oils
- production by body using tryptophan
Niacin function
- vasodilation
- decreased production of LDL
Niacin deficiency
- maize based diet
- tryptophan is bound and cannot be used to produce niacin
Pellagra
- niacin deficiency
- dermatitis (cassals necklace)
- diarrhea(atrophy of GI cells)
- dementia
- death
Pyrodoxine
- B6
- thermal labile substance, can be destroyed easily by heat
- some medications compete leading to deficiency
Medications that compete with Pyrodoxine
- Izoniazid (anti TB)
- Estrogens
- D-penicillamine (treatment of wilsons disease
Estrogens and pyrodoxine
-estogens have hyperplastic activity, promotes replication of cells in endometrium, could lead to cancer
symptoms of pyrodoxine deficiency
- cheilosis/cheilitis
- glossitis
- peripheral polyneuropathy
- convulsions
- increased sloughing of epitheleal cells
- nidus formatoin (urinary stones)
- dandruff
Seborrheic dermatitis
- dandruff
- sign of pyrodoxine deficiency
Cobalamin aka
B12 or cyan
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
Causes of B12 deficiency
- low animal product intake
- surgical removal of stomach
- malnutrition/alcoholism
- celiac disease
- antacids
- autoimmune
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
B12 function
-hematopoiesis
