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exam paper corrections Flashcards

1
Q

what blood tests are carried out to diagnose diabetes + give diagnostic reference ranges?

A

fasting plasma glucose (DM = >7 mmol/L)
HbA1c (48 mmol/mol or over)

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2
Q
  1. what is metabolic syndrome?
  2. how is metabolic syndrome diagnosed?
A
  1. group of disorders which increase risk of CVD: diabetes + raised fasting plasma glucose, abdominal obesity, hypertension + high cholesterol
  2. following results:
    * men with waist:hip ratio of >0.9 and women with waist:hip ratio >0.85
    * BP >140/90 mmHg
    * TAG >1.7mmol/L
    * fasting glucose >7.8mmol/L
    * HDL cholesterol <0.9mmol/L in men and <1mmol/L in women
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3
Q

what are macrovascular complications of diabetes melitus?

A

cardiovascular disease
peripheral vascular disease

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4
Q

what are 2 ways of treating hyperthyroidism?

A

carbimazole - stops iodination of thyroglobulin
surgical intervention - remove part of thyroid gland to reduce thyroid hormone production

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5
Q

what type of mutation occurs in sickle cells disease?

A

missense mutation
A is converted to T in 2nd base
glutamate is converted to valine

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6
Q

what happens in erythropoeisis?

A
  1. kidney senses hypoxia + increases production of erythropoetin
  2. erythropoetin acts on E-progenitor cells in bone marrow to produce more RBC
  3. new RBC transport more oxygen and this is detected by the kidney
  4. kidney decreases erythropoetin production
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7
Q

what is a sickle cell crisis?

A
  1. in a deoxygenated state HbS is exposed to deoxygenated conditions which results in sickling
  2. sticky hydrophobic pockets form allowing deoxy HbS to polymerise
  3. blocks capillaries resuliting in ischaemia
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8
Q

what are the bonds in glycogen?

A

alpha 1-4 + alpha 1-6 glycosidic bonds

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9
Q

what is the function of cellulose in the GI tract?

A

increases surface area for metabolism
allows substances to stick to the surface so enzymes can find them easier

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10
Q

what are the different layers of the mucosal wall of small intestine?

A

refer to camera roll

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11
Q

what does acetaldehyde form?

A

acetate

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12
Q

how can acetaldehyde be toxic to the liver?

A

toxic to hepatocytes - loss of bilirubin - jaundice
unable to produce urea - ammonia builds up
decreased protein production
loss of ALT/AST so cant convert amino acids

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13
Q

what is the pathology of psoriasis?

A

increased proliferation of keratinocytes - accumulation of cells in stratum corneum

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14
Q

what is the function of glucose-6-phosphate dehydrogenase?

A

produce NADPH
produce ribose

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15
Q

what is the aetiology (cause) of achondroplasia?

A

mutation in FGF3 receptor gene - normally promotes collagen formation from cartilage

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16
Q

what is endochondral ossification?

A

formation of bone through interstitial growth of hyaline cartilage

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17
Q

what are the effects of thyroid hormone in the body?

A

increase BMR and heat production - through increase num and size of mitochondria and increased synthesis of enzyme involved in respiratory chain
sympathomimetic effects - increase target cell response to catechalomines by increasing receptor number
stimulates metabolic pathway - stimulates lipolysis and beta oxidation of fatty acids, insulin dependent entry of glucose into cell + increase gluconeogenesis and glycogenolysis

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18
Q

what causes addisons disease?

A

chronic adrenal insufficiency

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19
Q

how is addisons disease treated?

A

mineralcorticoids
corticosteroids

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20
Q

if a patient wants to adhere to their medication but cant because of stresses and other commitments, what is this known as?

A

unintential non-adherence
patient wants to adhere to treatment but is prevented from doing so by barriers outside their control

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21
Q

how can sickle cell anaemia be treated?

A

hydroxycarbamide (increases HbF levels)
antibiotics
folic acid suplements
blood transfusion

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22
Q

what process results in the formation of exocrine glands?

A
  1. growth signal received
  2. proliferation of cells occurs and extracellular protein degradation enzymes produced
  3. epithelial cells invade spaces created
  4. central cells die off to produce a duct
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23
Q

in a patient with chronic kidney disease, what can result in anaemia?

A

uraemia - cant excrete urine as effectively
increase in urea decreases erythropoesiss and reduces lifespan of existing red blood cells as well as inhibiting platelet function

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24
Q

what is hereditary haemochromatosis?

A

autosommal recessive disorder which results in too much iron entering cells + accumulate in end organs causing damage
* affects the HFE gene
* HFE is normally involved reducing transferrin receptors affinity for iron-bound transferrin + it also promotes hepcidin which inhibits iron uptake through ferroportin

25
Q

what is pyruvate kinase defiency and what does it cause?

A

pyruvate kinase is the final enzyme in glycolysis
deficiency of this enzyme prevents glycolysis occuring in cells
this is extremely damaging to RBC which dont have a mitochondira and rely on glycolysis for ATP
this results in haemolysis of RBC = haemolytic anaemia

26
Q
  1. what is the method of inheritence of G6PD deficiency?
  2. why are RBC particularly affected in this condition?
  3. what abnormalitiy is seen on blood sample in G6PD deficiency?
A
  1. X-linked recessive
  2. only source of NADPH for these cells and are at increased risk of oxidative damage because they carry oxygen around the body
  3. heinz bodies - haemoglobin is cross linked due to inappropriate disulfide bonds forming
27
Q

what are the SLUDGE symptoms?

A

salivation
lacromation
urination
defication
GI upset
emesis

28
Q

what are the layers of the adrenal gland?

A

GFR:
glomerulosa (salt)
faciculata (sugar)
reticularis (sex)
salt: mineralcorticoids e.g. aldosterone
sugar: glucocorticoids e.g. cortisol
sex: androgens

29
Q

what are the different lateral adhesions systems for epithelia tissue?

A

most apical surface:
* tight junction - opens allowing small molecules
* adhesion belt - pairs and linked by actin filaments - stabalise tissue
* desmasomes - strongest adhesion - random pattern - spring like
* gap junctions - quickly allow communication between cells

30
Q
  1. which antibiotics inhibit cell wall synthesis?
  2. which antibiotics inhibit protein synthesis?
  3. which antibiotics inhibit cell membrane synthesis?
  4. which antibiotics inhibit nucleic acid synthesis?
A
  1. beta lactams + glycopeptides
  2. tetracyclines, aminoglycosides, macrolides
  3. polymixins
  4. quinolones
31
Q

what are the different groups of beta lactam antibiotics?

A

penicillins
cephalosporins
carbapenems
monobactams

32
Q

what are the different groups of glycopeptide antibiotics?

A

vancomyocin
bacitracin

33
Q

what are the different groups of antibiotics which inhibit nucleic acid syntheis?

A

folate synthesis inhibitors:
* sulfonamides
* trimethoprim

DNA gyrase inhibitor:
* quinolones

RNA polymerase inhibitor:
* rifampin

34
Q

what happens in endochondral ossification?

A
  1. Initial cartilage model
  2. Collar of periosteal bone appears in shaft
  3. Central cartilage calcifies, nutrient artery penetrate, primary ossification centre forms
  4. Medulla becomes cancellous bone, cartilage forms epiphyseal growth plates, epiphyses develop secondary ossification centres
  5. Epiphyses ossify and growth plates move apart, lengthening bone
  6. Epiphyseal growth plates replace by bone, hyaline cartilage persists
35
Q

what happens in itramembranous ossification?

A
  1. Small cluster of mesenchymal stem cells form a nidus
  2. MSCs become osteoprogenitor cells
  3. Osteoprogenitor cells become osteoblasts and lay down an extracellular matrix of Type I collagen (now, an osteoid)
  4. Osteoid mineralises to form rudimentary bone tissue spicules
  5. Spicules join to form trabeculae
  6. Trabeculae merge to form woven bone
  7. Woven bone is replaced by mature compact bone
36
Q

how is a bone fracture repaired?

A
  1. Haematoma formation - A blood clot (haematoma) is formed from which granulation tissue arises
  2. Fibrocartilaginous callus formation - procallus of granulation tissue is replaced by a fibrocartilaginous callus in which bony trabeculae are developing
  3. Bony callus formation - Endochondral and intramembranous ossification give rise to a bony callus of spongy/canccellous bone
  4. Bone remodeling - Cancellous bone is replaced by compact cortical bone until remodelling is complete
37
Q

what is the structure of cancellous bone?

A
  • The spaces are filled with bone marrow
  • Osteocytes lie between lamellae
  • No Haversian or Volkmann’s canals
38
Q

what is the primary action of cortisol?

A

increase lipolysis in adipose tissue

39
Q
  1. what is cushings syndrome?
  2. what can cause cushings syndrome?
  3. how is cushings syndrome treated?
  4. what are the symptoms of cushings syndrome?
A
  1. excessive amounts of cortisol
  2. adrenal adenoma or pituitary adenoma
  3. glucorticoids - hydrocortisone & prednisone
  4. symptoms:
    * increased proteolysis and gluconeogensis - polydipsia and polyria (steroid diabetes)
    * increased proteolysis causes muscle wasting - thin arms and legs
    * increased lipogensis of adipose tissue - moon shaped face and central obesity
    * defective protein structures - purple striae on lower abdomen, upper arms and thighs
40
Q

what is the difference between cushings disease and syndrome?

A

cushings syndrome - prolonged exposure to increased cortisol
cushings disease - specific case of a benign ACTH secreting pituitary adenoma

41
Q

how can dexamethasone indicate cushings syndrome?

A

dexamethasone is a drug given to determine cushings syndrome
dexamethasone would normally act on the pituitary gland to decrease ACTH release and therefore cortisol
however in patients with cushings cortisol remains high

42
Q
  1. what are the causes of too litle cortisol secretion?
  2. what is addisons disease caused by?
  3. what is secondary adrenal insufficiency caused by?
  4. what are the symptoms of too little cortisol?
A
  1. primary adrenal insufficiency (or Addisons disease) or secondary adrenal insufficiency
  2. failure of the adrenal gland to produce cortisol usually due to autoimmune disease
  3. failure of ACTH production, inadequate CRH production
  4. symptoms:
    * muscle weakness -
    * increased skin pigmentation - increase in ACTH as well as other products of POMC (α-MSH and γ-MSH) all of which stimulate melanocytes to produce more melanin
    * decreased BP - due to Na+ and fluid depletion
    * hypoglycaemic episodes
43
Q
  1. what is an addisonian crisis?
  2. how is an addisonian crisis treated?
A
  1. addisons disease causes a loss of both cortisol and mineralcorticoids when stressed symptoms worsen causing vomitting, severe dehyrdation, hypotension, confusion
  2. IV cortisol and fluid replacement
44
Q
  1. what is homocystinurias?
  2. what is method of inheritence of homocystinurias?
  3. what are the symptoms of homocystinurias?
  4. how is homocystinurias treated?
A
  1. defect in cystathione beta-synthase causes problems in breaking down methionine which causes excess homocystine to accumulate which is excreeted in urine
  2. autosomal recessive
  3. cardiovascular disease
  4. low methionine diet, avoid milk, meat, chees and eggs, cysteine, Vit B6 and B12 supplements
45
Q
  1. what is von gierkes disease?
  2. what are the symptoms of von gierkes disease?
  3. how is von gierkes disease treated?
A
  1. glucose 6-phosphatase deficiency which results in excess glycogen accumulation in tissues, however, glycogen is not broken down properly so causes hypoglycaemia
  2. constantly hungry, fatigue, irritability, puffy cheeks
  3. diet rich in carbohydrates, eat regularly
46
Q
  1. what is McArdle disease?
  2. what are the symptoms of McArdle disease?
A
  1. muscle glycogen phosphorylase deficiency
  2. muscle cramps, fatigue, weakness, exercise intolerance
47
Q
  1. what is phenylketonuria?
  2. what method of inheritence is PKU?
  3. what are the symptoms of PKU?
  4. how is PKU treated?
A
  1. phenylalanine hydroxylase is deficient so phenylalanine isnt converted to tyrosine. This means phenylalanine is converted to phenylpyruvate which results in the accumulation of phenylketones
  2. autosomal recessive
  3. severe intellectual disability, developmental delay, seizures, hypopigmentation
  4. low phenylalanine diet with lots of tyrosine, avoid artificial sweetners, avoid high protein foods
48
Q
  1. what is myasthenia gravis?
  2. what symptoms are commonly associated with myasthenia gravis?
  3. how is myasthenia gravis diagnosed?
A
  1. autoimmune condition which disrupts signals between nerves and muscles causing muscle weakness in the eyes
  2. droopy eyelids, double vission, slurred speech
  3. blood test, CT or MRI
49
Q

what is the pattern of inheritence of G6PDH deficiency?

A

x linked recessive

50
Q

what is the function of NADPH?

A

production of glutathione - protects against oxidative damage
reducing power for biosyntheiss e.g. fatty acid syntheis

51
Q

why are red blood cells particularly affected by G6PDH deficiency?

A

only source of NADPH in these cells
RBC at increased risk of oxidative damage since they carry oxygen around the body

52
Q

what are three differences between globular and fibrous proteins?
1. shape:
1. purpose:
1. solubility:

A
  1. shape: G = round F = long and narrow
  2. G = functional F = structural
  3. G = soluble in water F = insoluble in water
53
Q

what are 3 examples of DNA damage?

A

mismatch
deamination
single strand breaks

54
Q
  1. what is DNA replications stress?
  2. how does repetitive DNA (e.g. in huntingtons with CAG) cause replication stress?
A
  1. inefficient replication which results in replication fork slowing, stalling and/or breaking
  2. repetitive DNA can lead to fork slippage, if template strand has repetitive DNA + loops out there is forward slippage + DNA polymerase will miss out nucleotides
55
Q

how does base excision repair occur?
(this is specific to huntingtons)

A
  1. deamination converts cytosine base into uracil
  2. uracil is detected and removed, leaving a base less nucleotid
  3. leaving a hole in the DNA backbone
  4. this is then filled with the right base by DNA polymerase and the gap is sealed by DNA ligase
56
Q

which oncogene is targeted in breast cancer and what drug is used?

A

HER-2 gene is targeted by trastuzumab (Herceptin)
Up to a quarter of breast cancers have gross over-expression of the HER-2 gene and Herceptin can block Her-2 signalling

57
Q

what oncogene is targeted in chronic myeloid leukaemia and what drug is used?

A

oncogenic fusion protein (BCR- ABL) is targeted by imatinib (Gleevec)
imatinib inhibits the fusion protein

58
Q

tumour markers are released by different tumours, identify the tumour markers for the following cancers:
1. testicular tumours
1. hepatocellular carcinoma
1. prostate carcinoma
1. ovarian cancer

A
  1. human chorionic gonadotropin
  2. alpha fetoprotein
  3. prostate-specific antigen
  4. CA-125
59
Q

what are the hallmarks of a cancer?

A
  1. Self sufficiency in growth signals
  2. Resistance to growth stop signals – TSG’s
  3. Cell immortilisation (no limitation on the number of times a cell can divide)
  4. Sustained ability to induce new blood vessels (angiogenesis)
  5. Resistance to apoptosis
  6. Ability to invade and produce metastases

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