Pathology Flashcards

1
Q

What is the normal range of weight for the spleen?

A

100-250g

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2
Q

Where are macrophages and dendritic cells in the spleen located?

A

In the marginal zone

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3
Q

Where is Splenomegaly felt?

A

Under the left costal margin

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4
Q

What are the causes of Splenomegaly?

A

C- Congestion
H- Haematological ex haemolytic anaemia,sickle cell
I - Infection ex EBV, HIV, malaria
N-Neoplasm -
A- Autoimmune -Rheumatoid arthritis
S- Storage disease

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5
Q

True or False? Alkalines increase iron absorption?

A

FALSE!! Alkalines example ( Antacids,Pancreatic secretions ) REDUCE iron absorption

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6
Q

True or False? A reduced hepcidin serum favours iron absorption

A

TRUE!!

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7
Q

What is the cause of Neuropathy in Vitamin B12 deficiency?

A

This is due to accumulation of S‐adenosyl homocysteine and reduced levels of S‐adenosyl methionine.

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8
Q

What is an essential factor in the conversion of Methylmalonyl - CoA to succinyl- CoA?

A

Vitamin B12

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9
Q

True or False? Folate is responsible for the conversion of homocysteine TO methionine?

A

FALSE!! Vitamin B12 is responsible for the conversion of Homocysteine to Methionine.

“12 is when we need to B @ H&M” H before M !!

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10
Q

What is the main disease associated with Thymic Hyperplasia?

A

Myasthenia Gravis

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11
Q

Thymomas are of what origin?

A

Epithelial origin

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12
Q

Why is Thymic hyperplasia associated with Myasthenia Gravis?

A

MG is a neuromuscular disorder with an auto immune component. The body forms antibodies to acetylcholine receptors ( anti-acetylcholine receptors) . In the body the Thymus produces these antibodies , so more antibodies produced , more cells needed to produce them resulting in Thymic Hyperplasia.

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13
Q

Fill in th blanks. “ Developmental thymic pathology are _____ &_____”

A

Agenesis - Absence of an organ, usually due to non-appearance of its primordium in the embryo.

Hypoplasia- Incomplete development of underdevelopment of an organ or a tissue

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14
Q

Fill in the blanks.” Acquired thymic pathology are ______, ________ &________”

A

Atrophy
Hyperplasia
Neoplasia

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15
Q

What type of cells are found in Hassall’s corpuscle?

A

Squamous cells

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16
Q

In what disease can thymic hypoplasia & agenesis be seen?

A

DiGeorge syndrome accompanied by parathyroid developmental failures.

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17
Q

What is Primary Thymic Hypoplasia?

A

Loss of thymus. Therefore thymus was incompletely formed during embryological development. As a result the individual still has B-cells but not T-cells.

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18
Q

What is Secondary Thymic Hypoplasia/Agenesis?

A

Bone marrow is hypoplastic which results in a more severe immune deficiency state because loss of precursor lymphocytes precludes the formation of both immature B and T cells. Results in SCID

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19
Q

What is the emrbryologic origin of the Thymus?

A

Third pharyngeal pouch

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20
Q

What are the contributing factors to Acquired thymic atrophy?

A

Age
Malnutrition
Stress
Terminal illness
Cytotoxic drugs

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21
Q

What other diseases can be seen with thymic hyperplasia?

A

Grave’s Disease
Addison’s Disease-
Sclerodoma
Rheumatoid Arthritis
Systemic Lupus Erythrmatosus

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22
Q

What is another name for Type I thymoma?

A

Invasive thymoma - cytologically benign but biologically aggressive

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23
Q

A Thymic carcinoma is known as?

A

Type II thymoma - cytologically and biologically malignant.

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24
Q

What is the most common location for a Thymoma?

A

Anterior mediastinal mass

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25
Q

What diseases are associated with Thymomas?

A

Myesthenia Gravis
Cytopenias - Pure Red cell applasia, Acquired hypo γ-globulinaemia
Auto-immune -Graves/ Pernicious anaemia/ SLE/ Rheumatoid/polymyositis
Superior vena cava syndrome
Good syndrome

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26
Q

What is the main cause of lymphadenopathy?

A

Acute or Chronic Reactive hyperplasia

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27
Q

What cells are found in the Paracortex and medullary sinus of lymph nodes?

A

Plasma cells and Memory B cells

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28
Q

Where are B - cell centroblasts ( small- non cleaved cells) made ?

A

In the follicles

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29
Q

At what locations do localised acute reactive hyperplasia occur?

A

Tonsils- In tonsilitis lymph hyperplasia occurs in response to pharyngitis.
Inguinal- Hyperplasia of these nodes are related to STD’s, cuts and bruises on the lower limbs
Enteric- During gastroentiritis lymph nodes in the mesentery are involved.

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30
Q

At what location do generalised acute reactive hyperplasia occur?

A

Thoughought the body. (All lymph nodes are enlarged)

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31
Q

What is the characteristic feature of Follicular hyperplasia?

A

Germinal centre

32
Q

What is the microscopic appearance of Acute reactive hyperplasia?

A

Red-grey
Intact capsule ± perinodal extension

33
Q

What are the patterns associated with Chronic Reactive hyperplasia?

A

1) Follicular (B cell) -associated with increase antibody production

2) Paracortical/ diffuse (T cell)- associated with viral infections and cytotoxicity

3)Sinus histiocytosis (macrophages)-cytokine effect in lymph nodes draining tumours

4)Combinations

34
Q

What are causes of Chronic reactive hyperplasia -Follicular ?

A

Rheumatoid arthritis
Toxoplasmosis
Early HIV infection
Castlemans disease

35
Q

What are causes of Chronic reactive hyperplasia -Paracortical / Diffuse ?

A

Viral infections (such as EBV, mono)
Certain vaccinations (e.g., smallpox)
Immune reactions induced by drugs (especially phenytoin).

36
Q

True or False? Chronic reactive hyperplasia ( Sinus Histiocytosis) is often is encountered in lymph nodes draining cancers and may represent an immune response to the tumor or its products.

A

TRUE!!

37
Q

What are the main characteristics of Chronic reactive hyperplasia - Sinus Histiocytosis ?

A

Hypertrophy of lining endothelial cells and an infiltrate of macrophages (histiocytes).

38
Q

In which pattern of Chronic reactive hyperplasia has the presence of Tingible body macrophages?

A

Follicular hyperplasia

39
Q

What type of cells are present in reactive follicles in Follicular- Chronic reactive hyperplasia?

A

Scattered B cells
Scattered T cells
Phagocytic macrophages containing nuclear debris (tingible body macrophages)
A meshwork of antigen-presenting follicular dendritic cells.

40
Q

In Hb C, what substitutions occur?

A

A structural variant of normal haemoglobin A (Hb A) caused by an amino acid substitution of glutamic acid with lysine

41
Q

Fill in the blanks.” In Hb E, structural variant of normal haemoglobin A (Hb A) caused by an amino acid substitution of lysine for glutamic acid at position _______of the beta haemoglobin chain.

A

Twenty six (26)

42
Q

What are disorders of Heme synthesis known as?

A

Porphyrias

43
Q

What is the most common porphyria and what is it’s etiology?

A

Porphyria cutanea tarda and it is caused by deficiency in uroporphyrinogen decarboxylase.

44
Q

What is a distinct feature of Porphyria cutanea tarda & Erythropoietic porphyrias ?

A

They give a red-brown colour in urine

45
Q

What percentage of your body is made of water?

A

60%

46
Q

What is Hyperaemia?

A

Arteriolar dilation, increased blood INFLOW.
“ since you’re hyper you can come IN’

47
Q

What is Congestion?

A

Venous dilation, decreased OUTFLOW.

’ you are congested so you have to come OUT’

48
Q

True or False? Hyperaemia is an Active process while Congestion is a Passive process.

A

TRUE!!

49
Q

What is Oedema?

A

Accumulation of interstitial fluid within tissues.

50
Q

What is the name of Generalised Oedema ?

A

Anasarca

51
Q

What are the respective names for localised oedema in the following locations:
1. Lungs
2. Pericardium
3. Abdomen

A
  1. Lungs -HYDROTHORAX (PLEURAL EFFUSION)
  2. Pericardium -HYDROPERICARDIUM (PERICARDIAL EFFUSION)
  3. Abdomen- ASCITES
52
Q

Which term would best describe internal bleeding from a ruptured liver haemangioma?

A

Haemoperitoneum

53
Q

A class 4 Haemmorhhage has what percentage of blood loss?

A

> 40%

54
Q

A Class 1 Haemorrhage has what percentage of blood loss?

A

Up to 15%

55
Q

What is the smallest bleed and what is the size?

A

Petechiae (1-2 mm)

56
Q

Haemarthrosis is a haemorrhage in which location?

A

In joint spaces

57
Q

What is the location of a Thrombus?

A

Intravascular

58
Q

What is the Macroscopic appearance of a Thrombus?

A

Granular
Firm but friable

59
Q

What microscopic characteristic is a distinguished feature of a Thrombus?

A

Lines of Zahn

60
Q

What are thrombi located in the in heart chambers or in the aortic lumen known as?

A

Mural thrombi

61
Q

True or False? A chicken fat appearance is seen in all extravascular clots.

A

TRUE!!

62
Q

True or False? A chicken fat appearance is seen in postmortem clots.

A

TRUE!!

63
Q

True or False? Postmortem clots are attached to the underlying vessel wall.

A

FALSE!! They are NOT attached.

64
Q

Fill in the Blanks.Platelets are involved in _______ while platelets are uninvolved in _______.

A

Platelets are involved in the formation of Thrombus
Platelets are uninvolved in the formation of Clots

65
Q

What are the components of Virchow’s Triad?

A

Hypercoagulbility
Endothelial Damage
Circulatory Stasis

66
Q

Thrombi present on the heart valves are called ?

A

Vegetations

67
Q

Congenital abnormalities and ex May-Thurner syndrome and Paget- Schrotter syndrome can affect which part of Virchrows triad?

A

Circulatory Stasis( Abnormal Blood Flow)

68
Q

Oestrogen therapy, Inflammation and Dehydration can affect can affect which part of Virchrows triad?

A

Hypercoagubility

69
Q

Physical trauma strain and Microtrauma to the blood vessel can affect which part of Virchows triad?

A

Endothelial Damage

70
Q

Arteriosclerosis and Increase homocysteine levels can affect what part of Virchow’s Triad?

A

Endothelial damage

71
Q

True or False? Oral contraceptive are associated with hypercoagubility.

A

TRUE!!

72
Q

In what organs are Anemic (White) Infarcts seen ?

A

Organs with end circulation
- Heart
- Spleen
- Kidney

73
Q

In what organs are Haemorrhagic (red) infarcts seen?

A

Organs with dual circulation
Liver
Small Intestine

74
Q

Where was the spleen developed from?

A

Dorsal mesogastrium

75
Q

When does the spleen begin to develop?

A

6th week

76
Q

What is the nerve supply of the spleen?

A

The spleen is supplied from the coeliac plexus with sympathetic fibres only.