Revision of MoD questions Flashcards
inherited angio-oedema
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.
chronic granulomatous disease
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
bradykinin
kallikrein converts it from kininogen
powerful vasodilator, inc.s vascular permeability, constricts SMCs, stimulates pain receptors
syphilis
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
results of an AIR
resolution, abscess, fibrosis/scarring, death
what do macrophages release?
interleukin, TNF-alpha
Marfan’s syndrome
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
what stain can be used to detect bacteria?
Ziehl-Nielsen (acid fast) - acid fast (mycobacterium) bacteria stain pink
systemic lupus erythematosus
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
wallerian degeneracy
nerve is cut, distal to the laceration the axon degenerates
cartilage healing
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
pressure ulcers
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
proud flesh
excessive amounts of soft, oedematous (excessive fluid inside) granulation tissue produced during healing of large surface wounds
warfarin mechanism of action
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)
immediate treatment of an MI caused by CAD
immediately: O2, morphine for pain, aspirin to reduce platelet clotting, organic nitrates for vasodilation
red infarct types
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
treatment/prophylaxis of arterial thrombus
streptokinase (esp. coronary)/aspirin
initiation of clotting cascade
prostacyclin
a prostaglandin which prevents adhesion and aggregation of platelets to endothelium
thrombomodulin
binds to any locally formed thrombin and this complex initiates the anti-coagulant effects of protein C and protein S
polycythemia
proportion of blood volume filled by Hb increases
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
a) hypertrophy of the endometrial uterine layer
b) breast development by hyperplasia -> hypertrophy, lactation
c) hypertrophy and plasia
psoriasis
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)
benign melanoma is called
naevi
idiopathic thrombocytopoenic purpura
thrombocytopenia (low platelets) but with normal bon emarrow and an absence of other causes of thrombocytopenia
cachexia cause
inc. TNF-alpha, cytokines -> feel unwell -> don’t eat -> weight loss
what may a) small cell carcinomas of lung, b) testicular teratomas and c) carcinoid tumours produce?
a) ACTH
b) hCG
c) 5-hydroxytryptamine (seritonin)
difference between skin cancers
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.
features of familial adenomatous polyposis
numerous polyps -> adenomous
reed sternberg cells
giant cell derived from B lymphocytes seen in individuals w/ Hodgkins lymphoma
b symptoms in hodgkin’s
fever, weight loss, night sweat
marker of more advanced disease
sequence of events in cervical epith -> invasive cervical carcinoma
infection -> viral oncogenes -> dysplasia -> CIN (cervical intraepithelial neoplasia, how far through cervix wall) I -> CIN III -> cancerous -> through BM -> squamous cell carcinoma
complications of a CIR
Tissue destruction, fibrosis, atrophy
complications of granulomatous inflammation in the bowel
fibrosis -> bowel stricture (narrowing) -> obstruction
CIR -> tissue damage through bowel wall -> perforation
2 local mediators important for stimulating collagen synthesis
TNF-alpha
TGF-beta (transforming growth factor)
