Circulation: Pathology

Front 1

Hypertension gen

Back 1

- long-term increase in BP for given CO
1. increased arteriolar constriction
2. increase in resistance: TPR or pulmonary
3. heart generates higher P to maintain normal BF

Front 2

primary hypertension

Back 2

-occurs without underlying reasons frequently in humans ( 95%)
- very rare in animals

Front 3

secondary hypertension

Back 3

-consequence of another primary disease

Front 4

secondary hypertension in dogs

Back 4

- frequent causes:
1. renal failure: elevated angiotensin and aldosterone cause vasoconstriction and NaCl retention, respectively
2. hyperadrenocorticism (cushing's):
- increased cortisol and aldosterone
- most frequent hormonal dysfunction in adult-old dogs

Front 5

secondary hypertension in cats

Back 5

-most frequent causes:
1. renal failure
2. hyperthyroidism:
a. thyroid gland produces excess of thyroxine
b. enhances the effects of Norepi and Epi

Front 6

local edema

Back 6

impressions remain after pushing on the edematous site

Front 7

puerperal gaseous edema

Back 7

clostridium novyi (anerobic) infection:
- produces toxins and gas
- toxins cause edema

Front 8

eyelid edema

Back 8

1. bilateral: long hospitilization in recumbent position
2. unilateral: insect bite

Front 9

edema causes

Back 9

- noticeable excess in interstitial fluid caused by imbalance between filtration/reabsorption/ lymph flow:
1. increased capillary hydrostatic P
2. decreased plasma oncotic P
3. lesion of capillary cell membranes
4. decreased lymph flow

Front 10

normal P dynamics of exchange in capillary bed

Back 10

1. arterial side: hydrostatic P of blood(driving force)> oncotic P of interstitium= filtration
2. venous side: oncotic P of blood (driving force)> hydrostatic P of interstitium= resorption

Front 11

normal % dynamics of exchange in capillary bed

Back 11

- 20 L/ day (humans): filtered from plasma into ECF
- 18L/day: reabsorped into plasma
- 2 L/day (10%): return to the circulation through the lymphatic system

Front 12

imbalance between filtration and resorption

Back 12

filtration exceeds resorption and lymph flow= edema:
1. increased venous P= increased filtration
2. decreased plasma oncotic P (eg hypoproteinemia)= decreased resorption

Front 13

factors which limit degree of edema

Back 13

1. filtration limited: by increase of interstitial hydrostatic P (no further flow increase above +2mmHg)
2. filtration reduced: by decrease of interstitial oncotic P
3. lymph flow promoted: by increase on interstitial hydrostatic P

Front 14

edema caused by increased venous P

Back 14

1. cardiac failure
2. pulmonary congestion

Front 15

edema due to cardiac failure

Back 15

- cause: increased venous P
- Left side: lung
- R side:
1. animals: abdomen
2. humans: legs

Front 16

edema due to pulmonary congestion

Back 16

- cause: increased venous P
-lung or legs/abdomen
-when lung interstitium is full, fluid is filtered into the air spaces and alveoli: cough of frothy fluid

Front 17

edema due to hypoproteinemia

Back 17

1. malnutrition: kwashiokor (humans) causes ascites
2. loss of protein:
a. nephrotic syndrome: glomerula permeable to proteins
b. severe burns: loss through damaged capillaries

Front 18

edema due to hypoxia

Back 18

mountain sickness:
-limited oxygen transport capacity
- 8-24 hours after first arrival at high altitudes (>3000m)

Front 19

edema due to lymphatic obstruction

Back 19

=lymphedema
1. tumor: location depends on tumor
2. parasites/ diseases: microfilaria, elephantitis, tuberculosis (TBC), pnuemonia

Front 20

hemmorrhage decreases

Back 20

1. BV (venous side)
2. CO
3. arterial P
4. central venous P
5. atrial P
6. hematocrit, nutrients, etc

Front 21

immediate control mechanisms of hemmorrhage

Back 21

-survival: return of arterial P within seconds to minutes
- S and PS nerves
- baro, chemo and volume receptors
- CNS ischemic mechanism

Front 22

intermediate control mechanisms of hemmorrhage

Back 22

-conservation: minutes to hours
1. vasoconstriction: BF to kidneys decreased via renin and ADH
2. vasodilation: stress relaxation mechanism= protect against high BP, lasts min- hours
3. capillary fluid shift mechanism:
low capillary hydrostatic P shifts fluid from interstitium to blood

Front 23

long term control mechanisms of hemmorrhage

Back 23

-restoration: hours to months
1. renal: BF decreased via renin
2. thirst: baroreceptor and atrial volume receptor reflexes trigger hypothalamus--> thirst --> 1-2 days
3. replacement of blood components:
a. plasma proteins: liver, days
b. blood cells: bone marrow, weeks

Front 24

effectiveness of renin in hemmorrhage

Back 24

- severe hemmorrhage: acute fall of BP to 50
- P compensation within minutes:
1. without renin: BP up to 60
2. with renin: BP up to 83

Front 25

circulatory shock definition

Back 25

-generalized inadequacy of BF throughout the body to extent that tissues are damaged

Front 26

effects and clinical signs of circulatory shock

Back 26

1. vasoconstriction: cold limbs (except in septic), pale skin
2. hypoxia: cyanosis (tongue, conjunctiva), flat respiration
3. low BP: threadlike pulse, oliguria (reduced urine)
4. sympathetic activity: mydriasis = dilated pupils

Front 27

classifications of circulatory shock

Back 27

1. hypovolemia
2. traumatic: burn, bruises= plasma loss
3. dehydration: diarrhea, peritonitis
4. anaphylactic: allergic= loss of plasma
5. toxic= vasomotor paralysis

Front 28

non- progressive stage of circulatory shock

Back 28

- reduction of blood supply to non-vital organs via vasoconstriction of ANS, catecholamines, hormones:
1. heart: baroreceptor reflex
2. kidney: renin
3. hypothalamus: ADH
4. suprarenal gland
- 40% loss of blood in dogs
- depending on severity full recovery possible without treatment

Front 29

progressive stage of circulatory shock

Back 29

decentralization of blood circulation
1. vasomotor failure
2. cardiac depression
3. nervous depression
- depending on severity, full recovery possible with treatment

Front 30

vasomotor failure in progressive circulatory shock

Back 30

oxygen and nutrient deficiency, plus increase of metabolic end products in tissues:
1. damage of capillary membranes
2. plasma shift to interstitium
3. decreased BV
4. increased blood viscosity: danger of thrombosis

Front 31

cardiac and nervous depression in progressive circulatory shock

Back 31

1. cardiac:
- decreasing arterial P decreases coronary circulation
- positive feedback cycle
2. nervous: oxygen deficiency effects CNS= clouding consciousness

Front 32

irreversible stage of circulatory shock

Back 32

decompensation of blood circulation:
cardiac failure and failure of cardiovascular centers:
1. too much tissue damage
2. too many destructive enzymes released into body fluids
3. too much acidosis
- no ability to recover, regardless of treatment or restoration of BP