Revision of MoD questions

Question 1

inherited angio-oedema

Answer 1

Hereditary angioedema is caused by a genetic mutation in the C1-esterase inhibitor (C1-INH) gene ->
the body does not make enough C1-INH protein -> increased bradykinin

Certain factors are thought to trigger hereditary angioedema, such as: trauma, including surgery or infection the oral contraceptive pill pregnancy

The mutated C1-INH gene is passed down through families in a pattern known as autosomal dominant inheritance.

Question 2

chronic granulomatous disease

Answer 2

inability of phagocytes to kill bacteria and fungi they have ingested, due to a defect in the NADPH oxidase comples that releases free radicals

S&Ss: initially involving the skin eg perianal, axillary, scalp abscesses

-other features include fever, diarrhoea, pulmonary abscesses and granulomas, spleen abscesses, liver abscesses, lymphadenopathy (swollen lymph nodes) and hepatosplenomegaly

Question 3

bradykinin

Answer 3

kallikrein converts it from kininogen

powerful vasodilator, inc.s vascular permeability, constricts SMCs, stimulates pain receptors

Question 4

syphilis

Answer 4

Treponema pallidum bacteria causes it

Primary: The initial symptoms of syphilis can appear any time from 10 days to three months after you have been exposed to the infection.

• easily overlooked painless sore/ulcer where the pathogen was transmitted that disappears w/in 2-6 weeks
• lymph node swelling in eg neck, armpit, groin

Secondary: common symptoms include headaches, tiredness, swollen lymph glands, non itchy rash on palms of hands/feet commonly

Latent (hidden stage): no symptoms

Tertiary: most dangerous, affects many places, eg dementia, strokes, numbness, paralysis, blind/deafness heart disease, skin rash

Question 5

results of an AIR

Answer 5

resolution, abscess, fibrosis/scarring, death

Question 6

what do macrophages release?

Answer 6

interleukin, TNF-alpha

Question 7

Marfan’s syndrome

Answer 7

disorder of CT caused by defect in gene fibrillin-1 which plays an important role as a building blockfor CT
also causes excessive growth of long bones, producing tallness, long arms and legs

Question 8

what stain can be used to detect bacteria?

Answer 8

Ziehl-Nielsen (acid fast) - acid fast (mycobacterium) bacteria stain pink

Question 9

systemic lupus erythematosus

Answer 9

SLE is a multi-system autoimmune disorder in
which auto-antibodies develop to DNA, RNA,
histone, blood cells, nerves and other body
constituents.

butterfly rash commonly seen on face

Question 10

wallerian degeneracy

Answer 10

nerve is cut, distal to the laceration the axon degenerates

Question 11

cartilage healing

Answer 11

Cartilage has limited repair capabilities: as chondrocytes are bound in lacunae, they cannot migrate to damaged areas. Therefore cartilage damage is difficult to heal. Also, because hyaline cartilage does not have a blood supply, the deposition of new matrix is slow. Damaged hyaline cartilage is usually replaced by fibrocartilage scar tissue

Question 12

pressure ulcers

Answer 12

large pressure to skin for small amount of time or vice versa, disrupts blood flow, ischaemia, skin starts to break down -> ulcer

tend to affect people who don’t move much eg bed ridden, also people w/ poor blood flow eg diabetes mellitus

Question 13

proud flesh

Answer 13

excessive amounts of soft, oedematous (excessive fluid inside) granulation tissue produced during healing of large surface wounds

Question 14

warfarin mechanism of action

Answer 14

inhibits carboxylation action of glutamyl carboxylase, diminishing the available vitamin K in the tissue -> coagulation factors cannot bind to phospholipid surfaces inside blood vessels -> anticoagulant

HOWEVER: not given for short term, as it promotes clot formation in the ST, by inhibiting prot C and S in first 36 hrs (S is a cofactor for C, worsening the problem)

Question 15

immediate treatment of an MI caused by CAD

Answer 15

immediately: O2, morphine for pain, aspirin to reduce platelet clotting, organic nitrates for vasodilation

Question 16

red infarct types

Answer 16

dual blood supply eg lungs - primary arteries occluded, secondary not enough to supply tissues

rich anastamoses eg intestines - capillary beds of two separate arterial supplies merge, leading to same situation as above

loose tissue eg lung - poor stromal support for capillaries -> more than usual haemorrhaging into dead cells

previous congestion eg congestive cardiac failure - heart cannot supply enough blood but there is still some being pumped

raised venous pressure - inc. press in veins -> hydrostatic pressure of arterioles < hydrostatic pressure of capillaries and tiss -> blood stasis -> infarction

Question 17

treatment/prophylaxis of arterial thrombus

Answer 17

streptokinase (esp. coronary)/aspirin

Question 18

initiation of clotting cascade

Answer 18

Question 19

prostacyclin

Answer 19

a prostaglandin which prevents adhesion and aggregation of platelets to endothelium

Question 20

thrombomodulin

Answer 20

binds to any locally formed thrombin and this complex initiates the anti-coagulant effects of protein C and protein S

Question 21

polycythemia

Answer 21

proportion of blood volume filled by Hb increases

Question 22

how does a) the uterus respond to high progesterone/oestrogen, b) the breasts respond to oestrogen in puberty and oxytocin and c) the prostate respond to high androgens

Answer 22

a) hypertrophy of the endometrial uterine layer
b) breast development by hyperplasia -> hypertrophy, lactation
c) hypertrophy and plasia

Question 23

psoriasis

Answer 23

T cells attack epidermal cells -> cell cycle speeds up in epidermis and T cells, immature cells reach the top layer too early -> die w/in 5-6 days due -> red, flaky, crusty patches covered w/ silver scales, causes itching and burning

treatments are topical, phototherapy and oral/injected medications (reduce prolfieration of skin cells, also target specific parts of IS)

Question 24

benign melanoma is called

Answer 24

naevi

Question 25

idiopathic thrombocytopoenic purpura

Answer 25

thrombocytopenia (low platelets) but with normal bon emarrow and an absence of other causes of thrombocytopenia

Question 26

cachexia cause

Answer 26

inc. TNF-alpha, cytokines -> feel unwell -> don’t eat -> weight loss

Question 27

what may a) small cell carcinomas of lung, b) testicular teratomas and c) carcinoid tumours produce?

Answer 27

a) ACTH
b) hCG
c) 5-hydroxytryptamine (seritonin)

Question 28

difference between skin cancers

Answer 28

basal cell: the most benign and most common. Basal Cell skin cancer usually occurs on the face, neck, extremities and body parts that are exposed to the sun. It is a slow growing cancer that rarely metastasizes. Basal cell skin cancers can appear as a red patch of skin, a pearly bump, a scar–like lesion, or an open sore that does not heal.

squamous cell: more invasive than basal cell types and constitute about 20 percent of skin cancer cases. Squamous cell skin cancers commonly develop on the lower lip, on the edge of the lower eyelids, and extremities, but can occur anywhere. Squamous Cell skin cancers grow rapidly and can metastasize to other areas of the body if not removed, becoming life–threatening. This type of skin cancer can appear as a scaly red patch that might scab or bleed, an open sore that does not heal, or a raised, wart–like growth. Together, basal cell and squamous cell skin carcinomas constitute the vast majority of skin cancer cases. When caught early, these types of skin cancers have about a 95% cure rate.

Melanoma: the least common type of skin cancer but also the most dangerous and unpredictable. They can become very deadly, very quickly. Melanomas often occur in areas that have endured severe sunburns, though they can also occur in skin that has not had significant sun exposure. Melanoma skin cancer can also develop in moles that have been present for decades. About 30 percent of melanoma skin cancer cases develop in moles, and the other 70 percent in normal skin. They can occur on the bottom of the foot and even the retina of the eye.

Question 29

features of familial adenomatous polyposis

Answer 29

numerous polyps -> adenomous

Question 30

reed sternberg cells

Answer 30

giant cell derived from B lymphocytes seen in individuals w/ Hodgkins lymphoma

Question 31

b symptoms in hodgkin’s

Answer 31

fever, weight loss, night sweat

marker of more advanced disease

Question 32

sequence of events in cervical epith -> invasive cervical carcinoma

Answer 32

infection -> viral oncogenes -> dysplasia -> CIN (cervical intraepithelial neoplasia, how far through cervix wall) I -> CIN III -> cancerous -> through BM -> squamous cell carcinoma

Question 33

complications of a CIR

Answer 33

Tissue destruction, fibrosis, atrophy

Question 34

complications of granulomatous inflammation in the bowel

Answer 34

fibrosis -> bowel stricture (narrowing) -> obstruction

CIR -> tissue damage through bowel wall -> perforation

Question 35

2 local mediators important for stimulating collagen synthesis

Answer 35

TNF-alpha

TGF-beta (transforming growth factor)