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B3 Flashcards

1
Q

Describe the aetiopathogenesis of iron deficiency anaemia

A

A) Increase iron demand -childhood and pregnancy
B)Increased iron loss - chronic blood loss , peptic ulcer and carcinoma
C) Decrease iron absorption - Malnutrition , Malabsorption
D) Decreased intake - poverty , elderly

  1. Hypochromic RBC ( Less Hb in each RBC)
  2. Microcytic RBC ( Less Hb in erythroid precursors , more number of cell divisions , small size of RBC )
  3. Erythronium hyperplasia in bone marrow ( Tissue hypoxia , Increased erythropoietin )
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2
Q

Analyse and describe the laboratory diagnosis (blood , bone marrow and biochemical findings) of iron deficiency anaemia

A

Low Hb, low hematocrit , low RBC count
Platelets -increase
Reticulocytes count -low
**Peripheral smear - microcytic hypochromic, pencil cell , target cell
**Bone marrow - erythroid hyperplasia , micronormoblasts , Staining with Pearls Prussian blue stain to detect marrow iron stores

  • **Biochemical findings
  • low serum iron , low ferritin , high serum iron binding capacity , low transferrin saturation , low hepcidin : reduced iron stores inhibit it’s synthesis
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3
Q

Explain the clinical features of iron deficiency anaemia including epithelial changes

A

Features of anaemia : pallor of mucosa and skin, fatigue
B) Features of epithelial tissue change : Iron is required for integrity of normal epithelial tissue
Nail : Koilonychia (spoon shaped nails )
Tongue : Atrophic glossitis
Mouth : Angular stomatitis , angular chelitis

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4
Q

Describe the aetiopathogenesis of megaloblastic anaemia

A

Causes/Aetiology of Megaloblastic anaemia: Deficiency of Vit 12 & Folate

Pathogenesis :
A) Defects in DNA synthesis of blood in bone marrow.
B) Vitamin B12 & folate are essential form DNA synthesis
C) In deficiency state, hard to make DNA. RNA production as usual
D) Nuclear cytoplasmic asynchrony occur ( Nucleus development lags the cytoplasm.
E) Bone marrow give rise to Megaloblast.
F)In peripheral blood - macrocytes
G) Maturation defect is not restricted to the erythroid lineage (ineffective hematopoiesis)

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5
Q

Role of Vit B12 and folate

A

Vit B12 - Conversion methyltetrahydrofolate to tetrahydrohydrofolate
Methyltetrahydrofolate = form of folate receive by cells from plasma
Tetrahydrofolate is substrate for subsequent important reactions in cell

Folate - needed to form 5,10-methylene THF polyglutamate , coenzyme for thymidylate synthesis

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6
Q

Analyse and describe the laboratory diagnosis ( blood , bone marrow & biochemical findings) of megaloblastic anaemia .(C3)

A

A) Full blood count

  • Hb concentration reduced
  • Macrocytic anemia ( MCV>100)
  • Pancytopenia (Total WBC & platelets decrease )

B) Peripheral blood film

  • oval macrocytes
  • Howell-Jolly bodies ( nuclear remnant) in RBC
  • neutrophils with hypersegmented nuclei (more than 4 nuclear lobes)

C)Bone marrow
- Hypercellular , megaloblasts , giant metamyelocytes

D) Biochemical changes : increase unconjugated bilirubin , lactate dehydrogenase

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7
Q

Explain the clinical features of megaloblastic anemia including changes in other organs

A

Folate / Vit B12 deficiency

  • Anaemia with tinge of jaundice
  • Glossitis with smooth and shiny red raw beefy tongue
  • Neural tube defects in fetus
  • Sterility
  • Abnormal gonadal cell mitosis

Vit B12 deficiency

  • peripheral neuropathy
  • Optic atrophy
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8
Q

Define the atherosclerosis

A
  • Vascular disease characterized by formation of intimal lesion called atheromas , that protrude into vascular lumina
  • primarily effects elastic & muscular arteries.
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9
Q

Describe the aetiopathogenesis of atherosclerosis.

A

Pathogenesis
A) Endothelial injury :
Caused by : hemodynamic disturbance , hypercholesterolemia , inflammation , infection

Initiators : endotoxins , hypoxia , cigarette smoke , viruses

Causes : increase the endothelial permeability
: enhance leukocyte adhesion & altered gene expression

2) Smooth muscle cells proliferation and matrix synthesis
- activated platelets ,macrophages ,epithelial cell & SMooth muscle cell produce growth factors ( PDGF , FGF , TGF alpha.
- GFs cause proliferation of SMCs
- SMCs produce ECM and stabilised the atheroma( atherosclerotic plaque)

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10
Q

Describe the morphology of the atherosclerosis

A

Fatty Streaks
Gross :
begins as multiple minute yellow , flat spots that can coalesce into elongated streaks , 1 cm long or longer.

Histology :
Composed of lipid- filled foam cells, lymphocytes , extracellular lipids

Atheromatous Plaque 
Gross: 
-focal intimal thickening 
-lipid accumulation 
- white to yellow white in colour 
- encroach on lumen
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11
Q

Describe the site of the atherosclerosis

A 
\: Aorta - abdominal aorta > thrombus aorta 
\: coronary arteries 1st 6cm 
\: descending thoracic aorta 
\: Internal carotid arteries 
\: Circle of Willis
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12
Q

Describe the clinical significance (complications) of atherosclerosis

A

Depends on : Vessel effected & extend & confrigurationof AS change.

I) Slow insidious narrowing or vascular lumen causes ischaemia.
II) Sudden luminal occlusion by superimposed thrombosis or haemorrhage into plaque.
III) Thrombosis & embolism
IV)Weakening of vascular wall

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13
Q

Define isolated systolic hypertension and isolated diastolic hypertension

A
  • Isolated systolic hypertension is defined as a blood pressure >= 130mmHg systolic & <80mmHg diastolic
  • isolated diastolic hypertension is defined as < 130mmHg and >=80 mmHg diastolic
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14
Q

Classify hypertension.

A
  • Essential (primary) hypertension (90% of cases ) : idiopathic ( unknown cause)
  • Secondary hypertension : Causes
    A- aldosteronism
    B - bad kidney
    C - cardiac cause
    D - Drugs
    E- endocrine
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15
Q

State the classification of hemolytic anaemia

A

A) Intracorpuscular / Intrinsic
-Inherited
I) Membrane defect - hereditary spherocytosis
II) Enzyme defects -G6PD deficiency
III) Hemoglobinopathies - Thalassemia , Sickle cell disease

B) Extracorpuscular / Extrinsic
-Acquired
I) Immune mediated hemolysis - haemolytic disease of newborn
II)Trauma to RBC - defects cardiac valves

III)Infections -malaria

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16
Q

Explain the features of extravascular destruction of RBC

A

-in reticuloendothelial system

  • Spherocytes in peripheral blood
  • Increased serum LDH
  • increased indirect bilirubin
  • Increased urine urobilinogen
  • Increased fecal stercobilinogen
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17
Q

Explain the feature of intravascular of destruction of RBC

A
  • Fragmented RBC
  • Decreased in haptoglobin
  • Increased in LDH
  • 3 hemo : Hemoglobinemia , hemoglobinuria , Hemosiderinuria.
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18
Q

Define the thalassemia syndrome

A

Total absence or decreased synthesis of alpha or beta globin chains

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19
Q

State the types of thalassemia

A

Beta thalassemia :
Beta thalassemia major
Beta thalassemia minor
Beta thalassemia intermedia

Alpha thalassemia :
Silent carrier
Alpha thalassemia trait

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20
Q

Explain the Pathogenesis of Thalassemia

A

A) Impaired synthesis of beta chain and normal alpha chain synthesis
B) Alpha chain is not binding with beta chain
C) Free alpha chain
D) unstable aggregates
E) Damage to red cell membrane
F) Hemolysis

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21
Q

Explain the clinical features of thalassemia

A 
A) Onset after 6 months 
B) Anaemia 
C) Hepatosplenomegaly 
D) Growth retardation 
E) Skeletal changes - Cortical thinning , Malar prominence , Frontal bossing
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22
Q

Explain the lab diagnosis of thalassemia

A

A) Hematological changes

  • low Hb , HCt and RBC count
  • increase in reticulocyte count

B) Biochemical changes - High LDH & Unconjugated Bilirubin

C) Peripheral smear

  • Microcytic hypochromic
  • Target cell
  • Fragmented cell

D) Haemoglobin electrophoresis

  • Increased HbF ( 40-98%)
  • Increased Hb A2 ( 2-5%)
  • Decreased HbA

E) Bone Marrow

  • Erythroid hyperplasia
  • Increase iron stores
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23
Q

Define the sickle cell anemia

A
  • Inherited disease
  • Autosomal recessive
  • Due to point mutation
  • Substitution of valine for glutamic acid at the 6th position of beta globin chain
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24
Q

Explain the Pathogenesis of Sickle cell anemia

A

Properties of HbS

  • Soluble in the normal O2 tension
  • Low O2 tension —> polymerisation of HbS —> Crystalline form —> Sickle shaped RBC

Effects

  • Chronic haemolytic anaemia
  • Microvascular occlusion —> tissue infarction
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25
Q

Explain the lab diagnosis of Sickle cell anemia

A

A) Blood Parameters

  • Low Hb , Low HCt
  • Normal MCV , MCH
  • Increase in Reticulocytes

B) Peripheral blood

  • Anaemia
  • Sickle cell
  • Target cell
  • Heinz bodies
  • Polychromasia
  • Nucleated RBC

C) Bone marrow
- Erythroid hyperplasia

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26
Q

Explain about the Hereditary spherocytosis

A

A) Inherited disorder , Diverse mutations
B) Intrinsic defects in the red cell membrane skeleton
C) Red cell become spheroid
D) Less deformable
E)Splenic sequestration
F) Hemolysis

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27
Q

Explain the diagnosis of sickle cell anemia

A

A)Peripheral smear
B)Sickling test using sodium metabisulfite
C)Hb electrophoresis

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28
Q

Explain the lab diagnosis of Hereditary spherocytosis

A

A) Peripheral
Normocytic normochromic anemia
Increased Polychromatic cells
Many spherocytes

B)Confirmatory test
-Osmotic fragility test

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29
Q

Describe the aetiology of the tuberculosis

A

A) Typical organism for immunocompetent hosts

  • Mycobacterium tuberculosis
  • Mycobacterium bovis

B) Atypical organism in immunocompromised hosts

  • Mycobacterium Avium Intracellulae
  • Mycobacterium Kansasii
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30
Q

Describe the types of tuberculosis ( primary )

A

Primary tuberculosis
- occurring in patient who is not sensitised to tubercle bacilli

4 sites of Primary complex 
A) Lung - Ghon complex 
B) Small Intestine - Tabes mesenterica 
C) Oropharynx - Collar stud cold abscess
D) Skin- Lupus vulgaris
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31
Q

Describe the types of tuberculosis ( secondary )

A

Source

  • Endogenous : reactivation of a latent infection
  • Exogenous : reinfection

Pathogenesis

  • Acceleration of delayed hypersensitivity
  • Formation of abundant caseous necrosis
  • Extensive tissue destruction
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32
Q

Describe the types of tuberculosis ( miliary)

A
  • consequence of either primary or secondary TB which there is severe impairment of host resistance.
  • Widely disseminated disease , resulting in numerous small granulomas in many organs.
  • ** Favoured site : lungs , kidney , adrenal , bone marrow
    • Resistant sites : heart , thyroid & pancreas
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33
Q

Describe the factors that predispose to pulmonary tuberculosis

A
  • HIV infection : single most important risk for development of TB in HIV prevalent area.
  • Eldery patients , patients with AIDS , DM
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34
Q

Describe morphology ( histology) of rheumatic fever

A
  • Aschoff bodies
  • focal inflammatory lesion in the heart
  • composed of foci of T lymphocytes , occasional plasma cells & plump activated macrophages called Anitschkow cells ( a.k.a caterpillar cells )
    A) Have abundant cytoplasm
    B) Central round to ovoid nuclei (occasionally binucleate)
    C) Chromatin condenses into a central , slender , wavy ribbon.
    -Pancarditis
  • Diffuse inflammation of Aschoff bodies found in 3 layers of the heart ( pericarditis , myocarditis , endocarditis)
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35
Q

Describe the gross morphology of rheumatic fever

A

1) Fibrinous pericarditis - the fibrin strands in pericardial cavity ( opened) along with the pericardial membrane.
2) Inflammatory Vulvulitis is characterised by small vegetation ( verrucae)

3) Chronic / Healed phase
- Rheumatic mitral stenosis , calcification and fibrous bridging across the valvular commissures cause the narrowing (** fish mouth)

4) MacCallum plaques usually in the left atrium .
- irregular thickening induced by subendocardial lesions .

5) Right ventricular hypertrophy

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36
Q

List the various harmful effects of tobacco smoking.

A

A) Direct irritant effect : bronchitis

B) Carcinogenesis : risk of oral , laryngeal and oesophagus cancer

C)Atheroclerosis & myocardial infarction

D) Maternal smoking increase the risk of spontaneous abortions

37
Q

List the constituents of tobacco smoke and describe the its effects

A

Tar - carcinogenesis ( initiation of cancer )

Polycyclic aromatic hydrocarbons - carcinogenesis

Nicotine - Ganglionic stimulation & depression , tumour promotion

Phenol : mucosal irritation

Benzopyrene : Carcinogenesis

CO : Impaired O2 transport and use

Formaldehydes : mucosal irritation

Oxides of nitrogen : mucosal irritation

Nitrosamine : Carcinogenesis

38
Q

Define cardiac failure

A

A complex clinical syndrome in which the heart is unable to pump enough blood to meet the metabolic needs of the body

39
Q

Define the congestion heart failure

A
  • Congestion is a passive process which results due to impaired outflow of venous blood from a tissue
  • Inadequate pump function of the heart leads to congestion as fluid accumulates in lung and peripheral tissues
  • Common end point of many cardiovascular system
40
Q

State the characteristic of cardiac heart failure

A
  • reduced cardiac output
  • venous congestion
  • poor systemic perfusion
41
Q

Heart failure can be caused by ?

A

F - Faulty / defective heart failure
A - abnormal myocardial
I - ischemic heart disease
L - long standing hypertension

42
Q

Lists the causes of heart failures

A

A) Loss of muscle : Myocardial Infarction
B) Loss of contractility :Dilated cardiomyopathy
C) Pressure overload : Systemic hypertension , outflow obstruction ( aortic stenosis )
D) Volume overload : regurgitate valves

43
Q

Classify the heart failure

A

A) Based on duration

  • Chronic heart failure
  • Acute heart failure

B) Based on ejection fraction

  • systolic heart failure
  • diastolic heart failure
44
Q

Explain about systolic failure and diastolic failure

A

Systolic failure - cardiac contractility is impaired
- Ejection fraction is reduced

Diastolic failure - impaired ventricular relaxation and filling ( causes less blood fills the ventricular) due to the stiff and no compliant myocardium
- ejection is preserved

45
Q

State the causes of systolic heart failure

A

A) decreased contractility / force of contraction (myocardial infarction)

B) Increased afterload ( stress on ventricular wall during systole )

46
Q

State the causes of diastolic heart failure

A
  • restrictive cardiomyopathy
  • myocardial fibrosis
  • cardiac amyloidosis
  • constrictive pericarditis
47
Q

Explain the Pathogenesis of pulmonary TB

A

A) Entry into macrophages
- enter macrophages by endocytosis ( mannose receptor bind lipoarabinomannan & complement receptor

B) Replication in macrophages
- replicates within the phagosomes by blocking fusion of phagosome & lysosome

C)Innate immunity
- people with polymorphism in the NRAMP1 gene , the disease may progress due to absence of an effective immune response

D) TH1 cell response
- TH1 cells produce IFN gamma ; critical mediator that enable macrophages contain the M tuberculosis

E) TH1-mediated macrophages activation and killing of bacteria

F) Granulomatous inflammation and tissue damage
-IFN gamma activate macrophages into epithelium’s cells that aggregate to form granulomas

G) Host susceptibility to disease

48
Q

List the causes of sialadenitis

A

A) Trauma , viral and bacterial infection
B) Most prevalent form is mucocele
C) Mist common viral cause of sialadenitis is mumps which affect the major salivary glands , particularly the parotid and other glandular organs as the pancreas and testes

49
Q

Explain about mucocele

A
  • often found on the lower lip
  • present as fluctant lower lip swellings with blue translucent hue
  • results from either blockage or rupture of a salivary gland duct , with consequent leakage saliva into the surrounding connective tissue stroma.
  • Histology : Mucoceles are pseudocysts lined by inflammatory granulation tissue or fibrous connective tissue and filled with mucin & inflammatory cells , particularly macrophages
50
Q

List the tumours of salivary gland tumours

A

Benign ———— ——> Malignant
A) Pleomorphic adenoma - Mucoepidermoid carcinoma

B) Warthin tumor - Acinic cell carcinoma

C) Oncocytoma -Adenoid cystic carcinoma

D)Canalicular adenoma - Adenocarcinoma

51
Q

Explain the morphology of pleomorphic adenoma

A
  • Benign tumours that consists of a mixture of ductal(epithelial ) , myoepithelial & mesenchymal cells ( mixed tumour )

Morphology :
Gross : rounded, well demarcated masses , encapsulated
: cut surface is gray white with myxoid and blue translucent areas of chondroid ( cartilage-like ) stroma

Histology : Background is loose myxoid and hyaline tissue containing islands of cartilage and rarely foci of bone
: Island of well differentiated squamous epithelium may also present
- No epithelial dysplasia or mitosis activity

52
Q

Explain the clinical feature of pleomorphic adenoma

A
  • Presents as painless, slow-growing , mobile , discrete mass within the parotid or submandibular areas
  • The rate of recurrence following parotidectomy is about 4%
  • Rates of malignant transformation in pleomorphic adenoma correlate with age of the lesion
53
Q

Explain about he morphology of warthin tumour

A

Gross : round to oval encapsulated masses , 2 to 5 cm in diameter and readily palpable within the superficial parotid gland.
: Pale gray surface punctuated by narrow cystic or cleft like spaces filled with mucinous or serous secretions and frequently narrowed by polyploid projection of lymphoepithelial element.

Histology
- The lining composed double layer of on optic cells , innermost is columnar while cuboidal cells occupy the outer layer

54
Q

Explain about the morphology of mucoepidermoid carcinoma

A

-Most common primary malignant tumour of salivary glands

Gross : Gray or white in colour with mucin filled cysts.
Histology : Demonstrates cords , sheets or cystic configuration of squamous , mucous , or intermediates cells that have squamous features and small to large mucus filled vacuoles

55
Q

Explain the clinical course of mucoepidermoid carcinoma

A

Clinical courses and prognosis of mucoepidermoid carcinomas reflects the histologies grade.

-Low grade tumours may invade locally and recur in about 15 % of cases but they rarely metastasize. The 5 - year survival rate is more than 90%.
- High grade neoplasms and intermediate-grade tumors are invasive and difficult to excise .
Up to 30% metastasize to distant sites , yielding a 5 year survival of only 50%.

56
Q

Explain the morphology of adenoid cystic carcinoma

A

Morphology
Gross : Small , poorly encapsulated , infiltrate , gray- pink lesions

Histology : composed of small cells with dark, compact nuclei and scant cytoplasm

57
Q

Explain the clinical courses of adenoid cystic carcinomas

A
  • unpredictable , slow growing tumors that tend invade perineural spaces
  • regularly recur
  • Adenoid cystic carcinomas arising in the minor salivary glands tend to have poorer prognosis than those arising in the parotid glands
58
Q

Describe the morphology of acinic cell carcinomas

A

-represent only 2% to 3% salivary gland tumours

Gross :
- well circumscribed and tan-yellow to pink mass with homogenous cut surface

Histology : Tumours composed of cell that resembles the normal serous acinar cells of salivary glands with small and round nuclei

59
Q

Define the infective endocarditis

A
  • Is a microbial infection of heart valves or the mural endocardium that leads to the formation of vegetations composed of thrombotic debris and organisms , often assciated with destruction of the underlying cardiac tissues
60
Q

Explain the aetiology of acute IE , subacute IE

A

Acute IE : cause by infection of a previously normal heart valve by a highly virulent organism ( Staphylococcus aureus ) that rapidly produces destructive lesions.

Subacute IE : caused by organism with lower virulence factors ( Streptococcous viridans ) that cause insidious infections of deformed valves with overall less destruction

61
Q

Explain the native valve endocarditis and prosthetic valve endocarditis

A

Native valve endocarditis

1) Staphylococous >40% ( S.aureus)
2) Streptococcus <40% ( Viridans ( oral is , mutans , bovis) ,enterococci
3) HÁČEK organism ( actinobacillus )

B) Prosthetic valves
- S . Aureus

62
Q

Describe the causes of Infective endocarditis

A

A) Bacteremia

  • Transient bacteraemia occurs when a heavily colonised mucosal surface is traumatised
    • Teeth : Dental extraction
    • Tonsillectomy
    • Operations involving the respiratory , GI or GU tract mucosa
    • Biliary tract surgery

B) Haemodynamic Factors
- Bacteria colonisation more likely to occur around lesions associated with high degrees of turbulence
Example : valvular stenosis

63
Q

Explain the Pathogenesis of infective endocarditis

A

A) Altered valve surface
B) Deposition of platelets and fibrin - non bacterial thrombotic vegetation
C) Bacteraemia : - Attach to platelet- fibrin deposits
—> covered by more fibrin
—> protected by neutrophils
—> ongoing multiplication of bacteria
—> mature vegetation

Vegetation causes 
A) Tissue Damage 
B) Emboli 
C) Immune activation  
D) Bloodstream infection
64
Q

State the clinical features of the infective endocarditis

A
  • Fever
  • Heart murmur
  • Splenomegaly
  • Osler nodes ( toes )
  • Janeway lesion ( palm)
  • Splinter haemorrhage ( nails)
65
Q

Define the ischaemic heart disease

A
  • Groups that related entities resulting from myocardial ischemia - an imbalance between myocardial supply ( perfusion ) and cardiac demand for oxygenated blood
66
Q

Explain the Pathogenesis of Ischaemic heart disease

A

Myocardial Ischaemic results from reduced blood flow due to obstructive atherosclerotic lesion in the epicardial coronary arteries .

  • There is a long period (up to decades of silent , slow progression of coronary lesions before the sudden onset of symptoms.
  • IHD is often the late manifestation of coronary atherosclerosis.
67
Q

What is the measure to protect the donor?

A
  • Age 17-70 years old
  • Weight above 50kg
  • Haemoglobin >13g/dl for men and 12 g/dl for women
  • Minimum donation of interval 12 weeks and 3 donation per year
  • Pregnancy and lactation excluded because of high iron requirement
68
Q

Explain the measure to protect the recipient

A
  • Donor Selection
  • Stringent arm cleaning
  • Microbiological testing of donations : HIV 1&2 , Hepatitis B&C , HTLV, CMV , Malaria.
  • Monitoring and testing of bacteria contamination
69
Q

What is the blood and blood components / products

A
  • Whole blood
  • RBC ( packed cells)
  • Platelets concentration
  • Buffy coat
  • Cryoprecipitate
  • Fresh Frozen plasma
  • Irradiated Blood Components
  • Recombinant and Plasma based Factor VIII , IX concentrates
70
Q

Describe the morphology ( Gross ) of the primary tuberculosis

A
  • Solitary lesion ( Ghon focus ) at the pleura.
  • **- Lower part of upper lobe or upper part of lower lobe because this focus receive the greatest volume of inspired air
  • Chessy yellow white caseous necrosis develops
  • Ghon complex = Ghon focus + regional tracheobronchial lymph nodes
71
Q

State the gross morphology of secondary pulmonary TB

A
  • Involve apex of upper lobe of one or both lungs.
  • Sharply circumscribed , firm and gray white to yellow in colour.
  • In immunocompetent individuals —> undergoes progressive fibrous encapsulation —> fibrocalcific scars

**- 2 special features are extensive caseous necrosis and cavitation.

72
Q

Describe the histopathology of Primary Pulmonary TB

A 
Immunocompetent host ( Granulomas formation ) 
- Soft tubercles are seen ( central area of acidophillic , amorphous , acellular granular caseous necrosis surrounded by a rim of epitheliod cells , multinucleated Langhans & foreign body giant cells , lymphocytes and fibroblasts.

Hard tubercles are also seen as granulomas formation with absence of caseous necrosis

Immunocompromised host

  • Absence of granulomas formation
  • Abundant caseation necrosis poor in epitheloid cells & lymphocytes and numerous AFB ( non reactive TBj
73
Q

Describe the histopathology of secondary pulmonary TB

A
  • Active lesion show characteristic coalesce ttubercles with central caseation

**- Tubercle bacilli can often be identified with acid fast stains in
: early exudates and caseous phases of granulomas formation
: too few to be found in the late , fibrocalcific stages

74
Q

Explain the complications of Primary Pulmonary TB

A
  • Non progressive primary TB becomes arrested and healed
  • Ghon focus / complex undergoes fibrous scarring , dystrophic calcification
  • Reactivated , serving as a source of secondary TB
  • Progressive primary TB with lympho- haematogenous spread : Miliary TB
75
Q

Explain the complications of secondary pulmonary Tb

A
  • Fibrocalcific scarring
  • Involvement of pleura - pleural fibrosis , pleurisy with effusion & Tuberculous empyema,
  • Miliary TB
  • Potts spine
  • Amyloidosis
76
Q

Explain the Pathogenesis of rheumatic fever

A
  • Direct toxic effect of enzymes released form streptococci ( Streptolysin )
  • Inflammation triggered by similarity between Streptococcal pyogenes M proteins and cardiac muscle and cardiac valves —> molecular mimicry
  • Antibodies produced against M protein of Streptococcus pyogenes cross react with cardiac muscle Ag —> Ab- Ag complex formed —> activation of complements —> and recruits Fc receptors – bearing cell ( neutrophils and macrophages) —> macrophages activation —: inflammation
  • CD 4+T cell cross react with streptococcal Ag —> cytokines released —> macrophage activation —> inflammation
  • Combination of Ab and T cell - mediated reaction —> damage to heart tissue
77
Q

Explain the clinical features of Rheumatic fever

A
  • Diagnosis of RF based on clinical history and revised Jones Criteria
  • Presence of 2 major / one major and 2 minor manifestation.

Major Manifestation

  • Migratory polyarthritis of the large joints
  • Pancarditis
  • Subcutaneous nodules
  • Erythema marginatum ( irregular circulate skin rash)

Minor manifestation

  • Nonspecific signs and symptoms
  • Fever , arthralgia or elevated blood levels of acute phase reactants

***-Predominantly clinical manifestations are carditis and arthritis

Myocarditis can cause dilation , mitral valve insufficiency , heart failure
- May progress overtime to chronic rheumatic heart disease( RHD)

  • RHD is the only causes of mitral stenosis
78
Q

Describe the predisposing factor of the squamous cell carcinoma

A

5S

  • Smoking
  • Spirits
  • Spices
  • Sepsis ( infection of oral )
  • Sharp edge of tooth
79
Q

Explain the morphology of squamous cell carcinoma

A

Gross :

  • White patches or plaques
  • Ulcerated and protruding masses
  • Solitary or multiple
  • Verrucous plaques

Microscopy

  • well differentiated keratinising neoplasms to anaplastic poorly differentiated
  • Numerous nests of islands of malignant keratinocytes invading the underlying connective tissue stroma
  • Presence of keratin pearls
  • Well diffentiated

Dysplasia in leukoplakia —> carcinoma in situ —> squamous cell carcinoma

80
Q

Describe pyogenes granulomas

A
  • Inflammatory lesion on the gingiva of children
  • Lesion richly vascular and ulcerated
  • Red to purple colour
  • mature into dense fibrous masses and develop into an ossifying fibroma
  • Complete surgical excision is definitive treatment
81
Q

Explain about the aphthous ulcers ( Canker sores )

A

Common superficial mucosal ulcers

  • painful
  • cause :associated to celiac disease , inflammatory bowel disease
  • Ulcer are solitary or multiple , shallow with a hyperaemic base covered by a thin exudate
82
Q

Describe about left heart failure

A
  • Left heart failure = Lung failure
  • Impaired ability of the left ventricle to maintain adequate cardiac output

Forward failure : Reduced cardiac output

83
Q

What is formulae for the blood pressure?

A

Blood pressure = Cardiac output x peripheral resistance

84
Q

How renal factor influences Pathogenesis of hypertension ?

A

A) activity of the sympathetic nervous system
B) Activity of the renin - angiotensin - aldosterone system.
C) Genetic factor that control vascular tone and influence the reabsorption of sodium in the kidney

85
Q

Explain the pathological changes in various organ system due to hypertension

A

A) changes in blood vessels
: Accelerated atherosclerosis
: Hyaline arteriolosclerosis - homogenous pink hyaline associated with luminal narrowing
: Hyperplastic arteriolosclerosis - onion skinning of blood vessels ( malignant hypertension )

B)Flea bitten kidney : Small pin point haemorrhage on renal surface due to rupture of arteriolosclerosis and capillaries. Appear like flea bitten

C)Various cardiac pathologies :
I) Left Ventricular Hypertrophy - increased in peripheral resistance .This induced pressure overload of left ventricle . Cardiac myocytes undergo hypertrophy to generate more force to contraction.
II) Heart failure , Ischaemic heart disease , arrythimia

D) Hypertensive retinopathy -Arteriosclerosis of retinal

E) Intra cerebral haemorrhage
- Chronic hypertension leads to hyaline arteriosclerosis of blood vessels supply basal ganglia .This cause weakening of vessel wall and rupture

86
Q

State the complications of Ischaemic heart disease

A

A) Angina : Stable angina & Unstable angina

B) Myocardial Infarction : death of cardiac muscle cell due to lack of blood supply due to atherosclerosis.

87
Q

Explain the Pathogenesis of MI

A
  • is a area of necrosis of heart muscle resulting from a sudden absolute or relative reduction in the coronary blood supply
  • Most common precipitating cause is thrombosis superimposed on haemorrhage within , an atheromatous plaque
88
Q

State the complications of MI

A
  • Arrhythmias
  • Cardiac failure
  • Mitral incompetence
  • Myocardial rupture
  • Mural thrombus leading to embolism
  • Pericarditis

Pathology (4 decks)

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