Patho Week 1 Flashcards

1
Q

2 fundunmental item of pathological study

A
  • definition
  • aetiology
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2
Q

Objective of pathology study

A

1- ba able to correlate the clinical manifestation with the pathological changes
2- know prognosis of disease
3- realize the role of histopathology in diagnosis and treatment

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3
Q

Mention 4 lab pathological diagnosis

A

1- clinical suspicion : detailed clinical history

2- early diagnosis : Routine screening of asymptomatic individuals e.g:
- annual cervical smear
- monthly breast screen by mammography

3- cytological diagnosis : diagnosis of disease by examination isolated cells in body fluids e.g :
Exfoliated cells
Fine needle aspiration

4- Histopathological diagnosis : it is the definitive method in diagnosis

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4
Q

6 types of biopsy specimen

A

1- Excisional biopsy: ectomy
2- tru cut needle biopsy
3- Incisional biopsy “ punch biopsy “ ده الفتحات زي الفم والانف والrectum
4- Endometrial curetting
5- TUR : for urinary bladder and prostatic biopsy
6- Endoscopic biopsy: through GIt

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5
Q

6 techniques used to histopathological diagnosis

A

1- frozen sections
2- paraffin section: best material
3- immune peroxides ( immnuohistochemisty) : tumor antigens e.g : cytokeratin in epithelial tumor , vimentin in mesenchymal tumor
4- tumor marker ; CEA in GIT and breast tumor…… Alpha fetoprotein in hepatic carcinoma and PAP in prostatic

5- Electron microscopy: diagnosis of difficult types of disease
6- Molecular diagnosis:
PCR for chronic myeloid leukemia
Flow cytometry for measure DNA content

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6
Q

2 functions of fixation of specimen

A
  • preserve it from decay & autolysis
  • stabilize its integrity
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7
Q

7 causes of cell injury

A

1- hypoxia
2- physical agent
3- chemical agent
4- infection
5- immunological reactions
6- genetic derangement
7- nutritional imbalances

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8
Q

4 mechanism of cell injury

A

1- decrease energy production
2- imparied cell membrane function
3- increase Ca intracellular
4- accumulation of free radicals

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9
Q

2 causes and 2 effect of decrease energy production

A

Hypoxia , toxins
Failure of Na , K atp pump -> accumulating of water inside the cell

Increases anaerobic pathway -> increase lactic acid-> osmotic pressure

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10
Q

Causes and 2 effects of imapried cell membrane function

A

Activation of complement and production of free radicals

  • loss of structural integrity
  • defect in membrane preambility
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11
Q

What maintains Ca at low levels intracellular ?

A

Membrane energy dependent transport

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12
Q

What is the effect of increased Ca inside the cell

A

1- activations of phsopholipase lead to degrade membrane phospholipid
2- activation of protease -> break down proteins
3- Activation of Atpase -> depletion of ATP
4- Activation of endonuclease -> chromatin fragmentation

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13
Q

3 causes of production of free radicals and 3 effects

A

Radiation, chemical, reduction-oxidation reactions

Lipid damage, protein damage, fragmentation of cellular DNA and mitochondrial damage

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14
Q

What is the best evidence of necrosis and what does it include

A

Nuclear change
Pyknosis -> shrinkage and deeply stained

Karyorrhexis-> fragmentation of nucleus

Karyolysis -> dissolve of nucleus

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15
Q

2.Causes of acidophilia in necrosis

A

1- denatured protein has high affinity for eoisn
2- destruction of DNA lead to loss of affinity for basophill

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16
Q

5 types of necrosis and its cause and its common site

A

1- coagulative necrosis: most common due to sudden cutting of blood supply

2-liquefactive necrosis : the necrotic material undergoes softening due to the action of hydrolytic enzymes
e.g : 1- suppurative inflammation
2- lesion of brain and spinal cord

3- caseous necrosis : due to partial and slow liquefaction
E.g in tuberculous lesion caused by allergic reactions to protein of tubercule bacilli

4- fat necrosis
Enzymatic : due to action of lipase enzyme on fat of mesentry , omentum , abdominal fat which cause split the fat to glycerol and fatty acid , glycerol is absorbed in blood and fatty acid deposits with Ca as a small dull opaque white pathches

E.g : acute hemorrhagic pancreatitis

Traumatic ( non enzymatic ) : due to trauma and in ( breast , subcutaneous tissue)

5- fibrinoid necrosis : it affects wall of blood vessels and kidney glomeruli

Seen in 2 : autoimmune diseases, malignant hypertension

17
Q

4 fate of necrosis

A

1- healing by regenerating or fibrosis
2- cyst formation
3- dystrophic calcification
4- gangrene

18
Q

4 physiological and 4 pathological conditions of apoptosis

A

1- in Embryogenesis : interdigital cleft
2- Hormone dependent involution of tissue : endometrium during menstruation
3- maintains constant cell number ( normal cell turnover)
4- deletion of auto reactive cell

1- in viral infection: hepatitis
2- pathological atrophy after duct obstruction : pancreas
3- cell death in malignant tumor
4- elimination of cells with damaged DNA

19
Q

5 morphology of apoptosis

A

1- shrinkage of cells
2- condensation of chromatin
3- formation of apoptotic boides by fragmentation of cells and nuclei
4- phagocytosis by adjacent cells or macrophages
5- not accompanied by inflammatory reactions

20
Q

3 Mechanisms of intracellular Accumulation

A

1- Normal cellular substance produced at normal or increased level but the rate of metabolism is inadequate to remove it e.g fatty change

2- Accumulate of endogenous substances due to defect in metabolism: storage disease

3- Exogenous substances Accumulated because the cell can’t degrade or transport it : Carbon particles ( anthracosis)

21
Q

2 examples of clowdy swelling

A

1- renal convoluted tubules in nephritis
2- hepatocyte in viral hepatitis

22
Q

4 examples of hydropic swelling

A

1- epidermal cell in viral infection or mild burn
2- cell of renal tubules in electrolyte imbalance
3- hepatocyte in viral hepatitis
4- Beta cells of pancreas in DM

23
Q

Why fatty change ( steatosis) is more common in liver

A

Because it is the major organ involved in fat metabolism

24
Q

Mechanism of normal lipid metabolism in liver

A

FFA from adipose tissue or ingested food are transported to hepatocyte

In liver FFA are converted to TAG or cholesterol or phospholipid

Triglycerides are complexed with apoprotein to form lipoprotein to be released from liver to tissues

25
Q

5 mechanism of fatty liver

A

2 increase, 3 decrease

1- increase mobilization of FFA to liver in case of ( starvation , DM, increase fat intake)

2- increase rate of conversion from FFA to triglycerides ( alcohol consumption)

3- decrease metabolization of normal amount of fat ( disease of liver as viral hepatitis)

4- decrease oxidation of faty acid in case of hypoxia and anemia

5- decrease synthesis of apoprotein as in malnutrition, CCl4 , phosphorus toxicity

26
Q

Two types of Fatty change in heart

A
  • diffuse ( in toxic myocarditis diphtheria)
  • patchy ( in prolonged hypoxia as in severe anemia )
27
Q

Gross picture of heart in fatty change

A

Tigered effect ( yellow streaks of fatty cells and brown ones uninvolved)

28
Q

Fatty change of kidney

A

In cells of convoluted tubules
And it occurs secondary to kidney disease causing hypoxia to cells of convoluted tubules

29
Q

Compare between necrosis and apoptosis according to

1- causes
2- cell membrane
3- cellular content
4- morphology ( nucleus , cytoplasm)
5- inflammatory response

A

Necrosis :
Pathological , loss, enzymatic digestion, pyknosis, karyorrhexis , karyolysis , cytoplasm swollen and lysis , frequent inflammatory response

Apoptosis
Pathological, physiological
Intact , intact , fragmentation , shrinkage, no inflammatory response

30
Q

2 Effects of fatty change in liver

A

It depends on Cause and severity

1- If mild -> fatty change is reversible on cessation of the cause and may have no effect on cellular function

2- IF sever > Fatty change impair liver gnawed and may progress to liver cirrhosis and fibrosis

31
Q

3 types of fixative

A

Formaldehyde 10%
Alcohol eoxide 95%
Bouin for testicular biopsy