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CLS > Systems Pathology > Flashcards

Systems Pathology Flashcards

1
Q

New York heart association clsssifcation of heart failure

A

1 no limitation of physical activity
2 slight limitation ( breathlessness/fatigue)
3 marked limitation ( breathless with minimal exercise)
4 severe limitation- symptoms at rest

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2
Q

What bodily process makes heart failure worse

A

Renin release

adh- water retention

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3
Q

Explain cardiac remodelling

A

Hyper trophy in response to:
Adreneric - increases contractility and hypertrophy but causes myocyte apoptosis and toxicity
Angiotensin 11 - hypertrophy but causes changed ecxpression of contractile proteins
Cytokine TNFa - hypertrophy but remodelling of matrrix and dilation of chambers

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4
Q

What is left ventricular failure and what causes it

A 
Increases atrial pressure increased pulmonary pressure and SOB :
Acute ventricular dysrhythmias
Myocardial infarction and ischeamia 
Long standing hypertension 
Valve disease ( aortic/mitral) 
Cardiomyopathies and drugs 
Congenital heart diseases
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5
Q

What causes right ventricular heart failure and how does it manifest

A

Increased venous pressure, raised JVP and peripheral oedema- liver distension
Causes but left ventricular failure
Massive thromboembolism
Chronic disease- COPD chronic lung disease , pulmonary hypertension
Rare- valve disease

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6
Q

What is pulmonary hypertension caused by

A 
Emphysema 
Destroys alveolar walls 
Loss of lung Capps
Failure of lung ventilation
Hypoxia 
Pulmonary arteries constrict 
=hypertension
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7
Q

What is congestive cardiac failure

A

Combination of LVF and RVF
Commonly causes but ischeamic heart disease plus another cause of LFV
Also caused by cardiomyopathies ( primary gene defect in muscle protein, secondary toxins, metabolic disease, storage disease) and drugs

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8
Q

What are the two main problems in heart failure

A

Impaired function as a pump=
Fluid congestion
Inadequate blood flow to tissues

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9
Q

What is the general structure of the liver

A 
Heptocytes
Sinusoids
Portal tracts- aa portal vv and bile ducts
Central veins
Acinar architecture
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10
Q

What are the functions of the liver

A

Carbohydrate metabolism
fat metabolism
Protein synthesis - plasma proteins and catabolism
Bike synthesis- ( jaundice)
Storage or iron vitamins glycogen copper- (haemochromotosis)
Detoxification (drugs or hormone)

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11
Q

What are the different hepatocytes sensitive to

A

Centriole hepatocytes supplied by blood depleted in O2
- low oxidase activity
- high esterase activity
Peripheral hepatocytes- well supplied by oxygen
- low esterase activity

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12
Q

Name seven responses to liver injury

A

Fatty change
Hepatocyte necrosis
Cholestasis - alkaline phosphatase indicates
Inflammation
Fibrosis
Regeneration ( with fibrosis makes cirrhosis)
Neoplasia

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13
Q

What are the pathways to acute liver disease

A

Acute liver damage and systemic shock ( gram -ve sepsis) lead to severe liver cell necrosis
Decline in chronic liver disease might lead to acute decline.
Thesis both then lead to acute liver failure which can lead to liver necrosis

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14
Q

What does liver necrosis lead to

A 
Release of transaminase 
Failure of bilirubin metabolism 
Failure to detoxify nitrogenous compounds ( encephalopathy) 
Failure to synthesis factors 1972 
Shock with low GFR- renal failure
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15
Q

What are the causes of chronic liver damage

A

Hepatitis B C and D
Autoimmune disease
Drugs
Metabolic disease eg wilsons or a1 antitrypsin defiency

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16
Q

What is stage and grade of chronic hepatitis

A

Grade- severity of necrosis and inflammation

Stage- extent of fibrosis

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17
Q

What is cirrhosis

A

Fibrosis
Nodules of regenerated hepatocytes
Distorted liver architecture - not linked in cytoskeleton

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18
Q

What are the causes and consequences of cirrhosis

A

Chronic hepatitis and alcoholic liver disease
Reduced helatocyte function:
decreased synthesis of cogulation factors and albumin
Decreases secretion of bile
Decreased detoxification of nitrogenous compounds
decreased metabolism of steroid hormones
Portal hypertension: splenomegaly
Ascites
Porto-systemic anastomoses

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19
Q

What is jaundice

A

More than 50um bilirubin in plasma
Yellowing of skin, sclera and mucous membranes
Kernicterus- deposits in brain leading to nerve degeneration

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20
Q

What types of jaundice are there

A

Haemolytic
Intrahepatic
Obstructive
Physiological jaundice of newborn

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21
Q

What are the functions of the kidney

A

Excretion of nitrogenous waste
Salt ion and water homeostasis
Secretion of erythropoietin
Secretion of renin

22
Q

What does disease of the interstituim of the kidney lead to

A

Chronic kidney disease as it controls interstitial pressure and therefor reabsorption and secretion

23
Q

What damage could occur to the glomerular apparatus

A

Charges tbat repel proteins are lost and albumin can enter the filtrate

24
Q

How does under perfumed kidneys affect the tubule

A

Needs 02 for atp for active reabsorption

25
Q

What are the key features of acute renal failure

A

Oligourea or anuria
Electrolyte imbalance - hyperkalaemia and metabolic acidosis
Rising blood urea and creatinine

26
Q

What are the causes of active renal failure

A 
Pre- renal causation- reduced renal perfusion from 
shocks burns/bleeding/sepsis
Cardiac failure 
Intrinsic acute kidney disease 
A) tubulo-interstituim 
B) glomerular 
C) vascular 
Post renal active kidney injury
27
Q

What is tubulo-interstituim acute kidney disease

A

Necrosis of tubular epithelium due to reduced perfusion, no ion salt or water pumping takes places so the kidneys swell
Can recover from this

28
Q

What are the glomerular cause

Of acute kidney disease

A

Glomeruli nephritis
Immune complex mediated disease
Obliteration of glomerular lamina

29
Q

What are the vascular causes of acute kidney disease

A

Vasculitis- immune mediated inflammation and destruction of small vessels
DIC
Malignant tumour

30
Q

What is post renal acute kidney injury

A 
Acute obstruction of lower urinary tract 
In males- prostate/ureters
Females- ureters
Of lumen= stone
Wall= tumour of inflammation
Extrinsic= tumour/mass
31
Q

Define chronic kidney failure

A

Slowly progressive and irreversible loss of renal function due to irreversible destruction of a large number of nephrons

32
Q

What are the symptoms of chronic renal failure

A

Polyuria
Malaise/lethargy
Increasing ureamia confusion and eventual coma
Electrolyte imbalance- Na and water retention=hypertension

33
Q

What are the insisting factors to chronic renal failure

A 
Age
FH
Neohrotoxins
Diabetes mellitus
Urinary infection 
Primary renal disease 
Urinary obstruction
Cardiovascular disease
34
Q

What are the perpetuation factors for renal failure

A 
Hypertension
Proteineamia
Obesity
Anaemia 
Nephrotoxins
Cvd
Smoking
35
Q

What are the causes of renal failure

A 
congenital kidney disease (polycystic)
Chronic renal reflux 
Diabetic kidney disease 
Infection with hep B/C malaria TB or HIV 
Immunological damage to all glomeruli
36
Q

What pa02 and paCO2 define resp failure

A

O2 less than 8.0 kPa

CO2 more than 6.7kPa

37
Q

What are the lungs functions and what three mechanisms does it use to achieve these

A

Supply the body with O2
Remove major waste products
Ventilation, diffusion, and circulation

38
Q

What are the signs of resp failure

A

Resp compensation ( tachypnoea, accessory muscles, nasal flares, intercostal suprasternal or supra clavicle recession)
Increased sympathetic tone- tachycardia, hypertension, sweating
End organ hypoxia- altered mental state, confusion, disorientation
Bradycardia and hypotension
Hb desaturation - cyanosis

39
Q

What investigations could you do for someone who has resp failure

A 
Physical examination
Chest imaging 
FBC 
Arterial blood gases 
Urea and electrolytes
40
Q

What is type 1 respiratory failure

A

Hypoxeamia without hypercapnia
More common
Ventilation perfusion mismatch

41
Q

What is type 2 resp failure

A

Hypoxemia with hypercapnia

Ventilation problem

42
Q

What is V/Q mismatch

A

Low units- hypoxaemia and hypercapnia

High- wasted ventilation but doesn’t effect has exchange unless severe

43
Q

What causes v/q mismatch

A

Impaired diffusion - scarring - emphysema destroys Capp beds

Shunting - deoxygenated blood mixes with oxygenated blood which always results in less O2 content ( without hypercapnia)

44
Q

What are the causes of shunting

A

Pneumonia
Lung collapse
Severe pulmonary oedema

45
Q

What are the causes of type 1 resp failure

A 
COPD - chronic bronchitis and emphysema 
Pneumonia
Pulmonary odema
Asthma
Pulmonary embolism
Pneumothorax 
Broninchiestasis 
Pneumoconiosis- non organic dust 
Extrinsic allergic albeolitis
46
Q

What is COPD

A

Emphysema- dilation of alveolar due to destruction of walls in absence of scarring
Chronic bronchitis- excessive bro oval mucus plus cough

47
Q

What causes type 2 resp failure

A

COPD
Severe asthma
Drug overdose and poisoning

Primary muscle disorders
Head and cervical cord injury
Obesity
Pulmonary odema

48
Q

What are the types of resp 2

A

acute- minutes of hours with no compensation in acid base
Chronic- days- weeks
Hypercapnia- compensated with normalisation of blood pH and high bicarbonate
Hypoxia compensation with increased Hb and pulmonary hypertension

49
Q

What is cor pulmonale

A

Alveolar hypoxaemia caused by hypercapnia- constriction
Hypertrophy and hyperplasia of pulmonary smooth muscle
Increase in pulmonary resistance
Increasing after load of right ventricle- RVF and hypertrophy
Liver enlargement and peripheral odema

50
Q

What is the obstructive airway disease

A

FEV1 / FVC less than 0.75

Due to asthma or COPD

51
Q

what is restrictive airway diseas e

A

FEV1 /FVC normal or FVC is reduced

Fibrosis in the lungs- stiff lungs

CLS (12 decks)

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