Pathology Flashcards

(76 cards)

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
What diseases are associated with Thymomas?
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
26
What is the main cause of lymphadenopathy?
Acute or Chronic Reactive hyperplasia
27
What cells are found in the Paracortex and medullary sinus of lymph nodes?
Plasma cells and Memory B cells
28
Where are B - cell centroblasts ( small- non cleaved cells) made ?
In the follicles
29
At what locations do localised acute reactive hyperplasia occur?
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.
30
At what location do generalised acute reactive hyperplasia occur?
Thoughought the body. (All lymph nodes are enlarged)
31
What is the characteristic feature of Follicular hyperplasia?
Germinal centre
32
What is the microscopic appearance of Acute reactive hyperplasia?
Red-grey Intact capsule ± perinodal extension
33
What are the patterns associated with Chronic Reactive hyperplasia?
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
What are causes of Chronic reactive hyperplasia -Follicular ?
Rheumatoid arthritis Toxoplasmosis Early HIV infection Castlemans disease
35
What are causes of Chronic reactive hyperplasia -Paracortical / Diffuse ?
Viral infections (such as EBV, mono) Certain vaccinations (e.g., smallpox) Immune reactions induced by drugs (especially phenytoin).
36
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.
TRUE!!
37
What are the main characteristics of Chronic reactive hyperplasia - Sinus Histiocytosis ?
Hypertrophy of lining endothelial cells and an infiltrate of macrophages (histiocytes).
38
In which pattern of Chronic reactive hyperplasia has the presence of Tingible body macrophages?
Follicular hyperplasia
39
What type of cells are present in reactive follicles in Follicular- Chronic reactive hyperplasia?
Scattered B cells Scattered T cells Phagocytic macrophages containing nuclear debris (tingible body macrophages) A meshwork of antigen-presenting follicular dendritic cells.
40
In Hb C, what substitutions occur?
A structural variant of normal haemoglobin A (Hb A) caused by an amino acid substitution of glutamic acid with lysine
41
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.
Twenty six (26)
42
What are disorders of Heme synthesis known as?
Porphyrias
43
What is the most common porphyria and what is it's etiology?
Porphyria cutanea tarda and it is caused by deficiency in uroporphyrinogen decarboxylase.
44
What is a distinct feature of Porphyria cutanea tarda & Erythropoietic porphyrias ?
They give a red-brown colour in urine
45
What percentage of your body is made of water?
60%
46
What is Hyperaemia?
Arteriolar dilation, increased blood INFLOW. " since you're hyper you can come IN'
47
What is Congestion?
Venous dilation, decreased OUTFLOW. ' you are congested so you have to come OUT'
48
True or False? Hyperaemia is an Active process while Congestion is a Passive process.
TRUE!!
49
What is Oedema?
Accumulation of interstitial fluid within tissues.
50
What is the name of Generalised Oedema ?
Anasarca
51
What are the respective names for localised oedema in the following locations: 1. Lungs 2. Pericardium 3. Abdomen
1. Lungs -HYDROTHORAX (PLEURAL EFFUSION) 2. Pericardium -HYDROPERICARDIUM (PERICARDIAL EFFUSION) 3. Abdomen- ASCITES
52
Which term would best describe internal bleeding from a ruptured liver haemangioma?
Haemoperitoneum
53
A class 4 Haemmorhhage has what percentage of blood loss?
>40%
54
A Class 1 Haemorrhage has what percentage of blood loss?
Up to 15%
55
What is the smallest bleed and what is the size?
Petechiae (1-2 mm)
56
Haemarthrosis is a haemorrhage in which location?
In joint spaces
57
What is the location of a Thrombus?
Intravascular
58
What is the Macroscopic appearance of a Thrombus?
Granular Firm but friable
59
What microscopic characteristic is a distinguished feature of a Thrombus?
Lines of Zahn
60
What are thrombi located in the in heart chambers or in the aortic lumen known as?
Mural thrombi
61
True or False? A chicken fat appearance is seen in all extravascular clots.
TRUE!!
62
True or False? A chicken fat appearance is seen in postmortem clots.
TRUE!!
63
True or False? Postmortem clots are attached to the underlying vessel wall.
FALSE!! They are NOT attached.
64
Fill in the Blanks.Platelets are involved in _______ while platelets are uninvolved in _______.
Platelets are involved in the formation of Thrombus Platelets are uninvolved in the formation of Clots
65
What are the components of Virchow's Triad?
Hypercoagulbility Endothelial Damage Circulatory Stasis
66
Thrombi present on the heart valves are called ?
Vegetations
67
Congenital abnormalities and ex May-Thurner syndrome and Paget- Schrotter syndrome can affect which part of Virchrows triad?
Circulatory Stasis( Abnormal Blood Flow)
68
Oestrogen therapy, Inflammation and Dehydration can affect can affect which part of Virchrows triad?
Hypercoagubility
69
Physical trauma strain and Microtrauma to the blood vessel can affect which part of Virchows triad?
Endothelial Damage
70
Arteriosclerosis and Increase homocysteine levels can affect what part of Virchow's Triad?
Endothelial damage
71
True or False? Oral contraceptive are associated with hypercoagubility.
TRUE!!
72
In what organs are Anemic (White) Infarcts seen ?
Organs with end circulation - Heart - Spleen - Kidney
73
In what organs are Haemorrhagic (red) infarcts seen?
Organs with dual circulation Liver Small Intestine
74
Where was the spleen developed from?
Dorsal mesogastrium
75
When does the spleen begin to develop?
6th week
76
What is the nerve supply of the spleen?
The spleen is supplied from the coeliac plexus with sympathetic fibres only.