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Path. > Week 7 Part 1&2 > Flashcards

Week 7 Part 1&2 Flashcards

1
Q

ARTERIAL THROMBOSIS

A
  • thrombus in the arteries
  • most common
  • In the coronary artery
  • The patient can die.
  • The surface of the arteries looks rough
  • In cerebral artery
  • Results in death of the patient because it leads to development of ischemic stroke
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2
Q

VASCULITIS

A
  • inflammation of the vessels.
  • always results in swelling of the tissues- TUMOR.
  • the vascular wall may spread to the outside (but there is usually a lot of tissue outsidethat prevents it) so instead the lumen will get obstructed.
  • can be caused by autoimmune diseases.
  • ex. Temporal arteritis/ giant cell arteritis/ Horton’s disease
  • most common vasculitis that medicine knows.
  • characterized by headache and facial ache.
  • acute or chronic, often granulomatous, inflammation of the small to large arteries.
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3
Q

-granulomatous inflammation

A

characterized by development of multinucleated cells so this is also where it gets its name from

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4
Q

Horton’s disease

A

-inflammation of superficial temporal artery, ophthalmic and vertebral artery***

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5
Q

Polymyalgia rheumatic

A
  • this is muscle pain (not arthritis)
  • in the proximal portions of the pelvic and shoulder girdle
  • more common in ladies 50 years old and older.
  • this is associated with temporal arteritis.
  • this develops in 50% of people with temporal arteritis. (they go together)
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6
Q

VENOUS INFACRTION

A
  • ischemia means lack of BS to tissue (with arteries or veins)*
  • it happens in various types of hernia. Hernias are associated with displacement of organs from its own cavity to a different cavity
  • the most common hernia is in the intestines (stomach)
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7
Q

Para esophageal hernia

A

-part of the stomach goes between the esophagus and diaphragm (which is muscle and
can contract) –this may jam the small column where the stomach is up the stomach wallcontains BVs

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8
Q

Sheehan’s syndrome aka post partum syndrome (after delivery of the baby)

A

-infarction of the pituitary gland (anterior portion) (adeno hypophysis)
-normally, when the lady is pregnant she needs more and more hormones from pituitary gland. There is physiological hypertrophy of the anterior pituitary gland. After delivery
there is shrinking back to normal size.
-complications of delivery: you can get a hemorrhage from the uterus, blood is lost very
fast
-there is lack of blood to the pituitary and it dies forever.

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9
Q

Factors

affecting infarction

A

tissues innate vulnerability to hypoxia
pattern of vascular supply
the oxygen delivery capacity of the blood
rate of development of occlusion

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10
Q

tissues innate vulnerability to hypoxia

A
  • most is brain myocardium lungs, kidneys, spleen

- the more vulnerable for hypoxia are important organs for living.

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11
Q

pattern of vascular supply

A

-if one of the branches of an arterial tree is blocked it is bad and the area of the heartwill die
-if a person does lots of physical activity, they can develop collateral BVs which will
compensate when one branch is blocked. The portion of the heart will not undergo
infarcts.
-this helps us to survive.
-get anastomoses in the brain by studying and training your brain.

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12
Q

-ANASTOMOSIS

A
  • the union of branches of two or more arteries supplying the samebody region.
  • means coming together.
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13
Q

the oxygen delivery capacity of the blood

A
  • the RBC number in the blood
  • and if they can carry oxygen
  • we are talking about ANEMIA- decreased RBCs or decreases hemoglobin
  • if it is decreased, the oxygen carrying capacity of blood is decreased and these peopleare more susceptible to infarction.
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14
Q

rate of development of occlusion

A

-whether there is slow development of ischemia or if it develops immediately
-the science of ischemic heart disease develops when the occlusion is 75% or more of the coronary artery
-before 75%, no signs and symptoms are seen.
-but if you get 50% occluded at a faster rate, it may show signs and symptoms of
ischemia.

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15
Q

embolism

A

the sudden occlusion of a blood vessel by an EMBOLUS- an abnormalmass moving with the blood stream

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16
Q

Thromboembolism

A

-the most common type of embolism that occurs in the blood
-it is formed inside the blood vessels so that is why it is more common
-destruction of venous thrombus (each has a point of attachment to the vascular wall)
but on the veins it is loose- so portions of this can be torn apart from the major body of the thrombus and flow with the blood and result in obstruction

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17
Q

venous (thrombo) embolism

A

-goes to specific area of the body- lungs.
-if a thrombus detaches in the leg, the vessels get wider as they go to the heart. Thediameter is too large for the embolism to clog it so when it finally gets to the little
capillaries of the lungs it is stopped. (it is stopped in the lungs if it is in the venous
system**)

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18
Q

arterial (thomrbo) embolism

A

-they usually begin at the heart.
-it will go to the aorta without any problem because the diameter is large but it stops inthe small arteries of the brain (since they are smaller) ischemic stroke (more
common)

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19
Q

-source of embolites:

A

Thromboembolism: Mitral stenosis- artificial valves promotes thrombosis. Thesepeople need to take anti coagulants for the rest of their life
Bacterial endocarditis- complications= stokes

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20
Q

TYPES OF EMBOLISMS

A

fat embolism
air embolism
amniotic fluid embolism

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21
Q

fat embolism

A
  • develops when there is fracture of long bones
  • the bone marrow in long bones contains fat which bleeds from these spaces and goesinto venous circulation globus of fat is found in the lungs.
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22
Q

air embolism

A
  • dangerous if there is high amounts of air in the blood circulation
  • 10 ml of air will not change anything, it can be dissolved
  • 300 ml of air will kill people- presence of bubbles in the fluid prevents flow of the fluid*-results in air lock
23
Q

-bends aka caisson disease aka divers disease

A
  • develops in deep divers
  • deep down dramatic increase in pressure the nitrogen is dissolved in the blood
  • when people go up fast the pressure is less and less and the gas goes from dissolved to gas multiple obstruction of BVs
  • prevent this with slow ascent.
24
Q

amniotic fluid embolism

A

-fluid can not be embolism, but what is within the amniotic fluid can provoke embolism formation.

25
Q

Vitamins

A

-vita= in Latin means life
-amines means amines.
= amines of life.
-named by Kazimierz Funk

26
Q

Dr. Frederick Hopkins

A

Gave names for vitamins

Accessory food factors

27
Q

Umetro Suzuki

A

Discovered 1st vitamin in 1910

28
Q

water soluble

vitamins

A 
Thiamine
riboflavin
Niacin
Pyridoxine
(Cyan) cobalamin
29
Q

Thiamine

A
  • aka Vit B1.
  • it is located in the husks of grains.
  • if the grains are refined they will lack vit B1. (and all other vitamins)
  • refination of foods multiple epidemics  many deaths. (in china with rice)
30
Q

Deficiencies of Thiamine

A

Alcohol

beriberi

31
Q

Alcohol

A

they compete for the same receptors.-alcohol will remove thiamine from its binding

32
Q

-Beriberi

A

-associated with lack of B1
-described by Christiaan Eijkman
He found that the chicken who lived with people with the disease had
the same disease and wild chickens did not have it. So he thought there was something in the food

33
Q

dry beriberi

A
  • non specific peripheral polyneuropathy
  • with myelin degeneration (affects sensory, motor and reflex arch so you get the following:)
  • development of wrist drop, foot drop and first toe drop.
34
Q

wet beriberi

A
  • characterized by: enlargement of the heart
  • thinning of heart wall (flabby myocardium), weakened heart muscle-peripheral vasodilation (due to thinning of heart wall)
  • leads to cardiac failure (peripheral edema)
35
Q

Wernicke- kosakoff syndrome

A 
-two components: 
A. Wernicke encephalopathy 
-global confusion 
-apothy 
-listlessness 
-disorientation 
-ophthalmoplegia (the most important= eyes look in different directions) (usually a very bad neurological sign that shows the patient is close to death) 
B. korsakoff’s psychosis 
-anterograde amnesia 
  Forgetfulness about recent events 
  You can remember details from your past but you forget what happened a second ago (typical of beriberi) 
-inability to acquire new information  
  Result of thiamine deficiency 
-confabulation  
  This means the people always want to talk.
36
Q

riboflavin

A
  • vit B2

- deficiency occurs in debilitating people with chronic infections, cancer, TB

37
Q

ARIBOFLAVINOSIS

A

-cheilosis associated with the development of cheilitis
 Cracks in the angles of your mouth
 Bacteria goes there infection
 This is a degenerative process from B2 deficiency which switches to
inflammation (IT IS)
 It is primarily cheilosis and then goes to itis with inflammation (doesn’t need to get to itis if you cure it fast enough)

38
Q

-glossitis

A

Inflammation of the tongue
Lost of taste
Results in full atrophy- magenta colour.Always occurs with cheilosis

39
Q

-superficial interstitial keratitis

A

Normal: The cornea is transparent, it does not have blood vessels which allows usto see. It is fed through the tears. Tears must be high in nutrients to nourish the
cornea since it has no BVs.
Abnormal: development of BVs on the periphery of the cornea and they start to
grow into the center of the cornea.

40
Q

KERATISIS.

A

corneal inflammation

41
Q

-dermatitis

A

naso-labial fold – around the nose and

around the mouth. Another location is the cheeks, skin behind the ear and skin of scrotum/ vulva

42
Q

Niacin

A
  • vit B3 (in Russia is it called vitamin PP)
  • derivative of nicotinic acid nicotinamine (these are precurors)
  • the drug nitroglyercin is based on this. (this leads to vasodilation-vasodialtion in thevenous system and not the arteries)
43
Q

TRYPTOPHAN

A
  • maize (type of dark corn): tryptophan is bound to other things that can not be digested so tryptophan can not be the source of B3 for our gut flora.
  • some tribes that eat only corn develop B3 deficiency.
44
Q

-pellagra

A

vit B3 deficiency
-pelle aga= dry skin

-manifestations of pellagra: (disease of 3 or 4 D’s)
-Dermatitis
 Inflammation of skin in areas of the body that are exposed to the sun
 Arms, face, legs.
 On the neck is it called CASAL’S NECKLACE. (we have seen this before as primary nutrient deficiency)
- Diarrhea
 Inflammatory changes in the mucosa of the intestines.
-Dementia
 Loss of cognitive function
 Occurs due to degeneration of cerebral neurons* (especially the cortex)
-Death

45
Q

Pyridoxine

A

-vit B6
(1) thermally bile vitamin
-it undergoes destruction when it is warmed.
Izaniazid- anti TB medication
Estrogens- part of birth control pills. If you intake estrogen in high amount you can get B6 deficiency
D- penicillamine. Good chelating drug to remover copper (wilsons disease) (alsotreats systemic scleroderma)

46
Q

-manifestations of B6 deficiency:

A

-cheilosis
-glossitis
-convulsions in babies
- development of peripheral polyneuropathy
-*** development of SEBORRHEIC DERMATITIS
 Scaling of epithelial cells from the scalp due to decreased lifespan of epithelialcells
 These are greasy scales.
 Dandruff

47
Q

Nidus

A

B6 deficiency promotes formation of urinary tract stones which are formed around specific organic cords and is known as nidus
Stones of the urinary tract.

48
Q

(Cyan) cobalamin

A

Vit. B12
It has a special way to be absorbed*
Source of B 12 is animal food

49
Q

How B12 get absorbed

A 
the salivary 
glands produce R- binder whose function is to help B12 move further down the 
digestive tract in the stomach the B12 gets split (digestion) another R binder binds 
B12 in stomach to take it to the duodenum, they split again intrinsic factor of castle* is produced by the parietal cells of the stomach wall (this is the only place***) it 
carries B12 (aka extrinsic factor of castle) it travels through the jejunum to the ilium which contains special receptors for  intrinsic factors (not B12) then it goes into the 
blood circulation and they split again and is released from intrinsic factor.
50
Q

What causes vitamin B 12 deficiency?

A

-auto immune disease called auto immune chronic gastritis
There is production of the body of an antibody called parietal canalicular autoantibodies (type three antibody) they selectively kill parietal cells.
Blocking auto antibodies (type one antibody)
The antibody binds to the intrinsic factor site (epitote)
Binding auto antibodies (type two antibody)
They block receptors for intrinsic factor on ileum which has extrinsic factor on it.

51
Q

-pernicious (malignant) anemia

A

Killed millions of people
One type of MEGALOBLASTIC ANEMIAS
Auto immune disease

52
Q

B 12 deficiency anemia

A 
Inadequate dietary intake of vitamin B12
Surgical removal of stomach or ilium
Malnutrition or alcoholism
Celiac disease, Crohn's disease-disease of the ilium
Intake of some medications
Vegans
53
Q

Infarction

A

ARTERIAL THROMBOSIS.
VASCULITIS
VENOUS INFACRTION

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