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1st and 2nd year main conditions > 2nd year systems > Flashcards

2nd year systems Flashcards

1
Q

95% of colorectal cancers are transitional cell carcinomas - TF?

A

false. most bladder cancers are transitional cell carcinomas. (TCC) most colorectal cancers are adenocarcinomas

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2
Q

are most colorectal carcinoma’s familial or sporadic?

A

most colorectal cancers are sporadic with no familial or genetic influence. 10% will have a familial risk with HNPCC or FAP. 1% will have an associated underlying IBD.

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3
Q

name 5 risk factors for sporadic colorectal cancer

A
  1. smoking2. male3. age4. diabetes5. no exercise6. alcohol7. previous colorectal cancer
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4
Q

what type of cells do adenomas arise from?

A

adenomas arise from epithelial cells

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5
Q

what investigations would you like to carry out in CRC?

A

carry out an:1. proctoscopy2. colonscopy + picolax3. PET4. CT

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6
Q

in what stage of sleep are sleep spindles found?

A

stage 2

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7
Q

how does this stage 2 of sleep differ from stage 1?

A

stage 1 will have theta waves and eye movements. the waves are of low frequency in stage 1 and have a high amplitude.stage 2 will not have any eye movements. there are also sleep spindles in stage 2 and there are lower frequency of waves.

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8
Q

what type of waves occur in stage 3 and stage 4 of sleep?

A

delta waves will occur in both stage 3 and stage 4 sleep

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9
Q

low amplitude waves are found in stage 4 sleep. true or false?

A

false. stage 4 sleep has exclusively delta waves that have a low frequency but high amplitude

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10
Q

why is REM sleep described as being paradoxical?

A

the EEG pattern will mimic that of someone who is conscious and stressed. their waves have a high frequency and a low amplitude. it is possible that the person would be dreaming.

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11
Q

describe the 3 stages in bronchoalveolar epithelial stem cell transformation in cancer

A
  1. atypical adenomatous hyperplasia2. adenocarcinoma in situ3. invasive adenocarcinoma.this process is not linked to smoking
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12
Q

name a gene associated with Crohn’s disease

A

NOD2 geneside note just remember that Crohns disease and ulcerative colitis both have extra-intestinal manifestations

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13
Q

what genes are implicated in ulcerative colitis?

A

HLA genes

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14
Q

what antibody test can be done for ulcerative colitis?

A

anti-neutrophilic cytoplasmic antibody (p-ANCA)75% of ulcerative colitis patients will have the pANCA but only around 11% of CD patients will have the pANCA antibody.

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15
Q

to what degree will the serosal layer of the colon be involved in the inflammation of ulcerative colitis?

A

the serosal layer is minimally involved - only the mucosal layer is generally involved.ulcerative colitis also doesnt have any granulomas but crohns disease does

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16
Q

what layer of the gut tube will UC affect?

A

the mucosal and submucosa (at a push) layer

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17
Q

suggest 3 symptoms of radiation colitis?

A
  1. anorexia2. abdominal cramps3. diarrhoea4. malabsorption
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18
Q

high grade dysplasia is invasive - TF?

A

falsehigh grade dysplasia will result in carcinoma in situ crowded and very irregular. it is not yet invasivelow grade dysplasia will have an increased nuclear number, size and reduced colonic dysplasias are called adenocarcinomas.

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19
Q

Give 3 presentations of left and right sided colorectal adenocarcinoma

A

Right sided1. exophytic/lymphoid2. altered PR blood (anaemia)3. vague pain4. weakness5. obstructionLeft sided1. annular2. bleeding3. fresh PR blood4. altered bowel habit5. obstruction

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20
Q

a rapidly rising creatinine is associated with which type of glomerulonephritis?

A

crescentic glomerulonephritis is associated with a rapidly rising creatinine kinase

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21
Q

what is the filtration like of this type of GN?

A

there is cellular proliferation and the influx of macrophages in Bowman’s space. there will also be endothelial damage and fibrin deposition all accumulating to the main effect of no filtration.

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22
Q

describe 3 types of GN

A
  1. Diabetic GN - IgA will cause the proliferation of mesangial cells causing Kimmelsteil Wilson lesions with crushed capillaries.2. IgA GN- IgA stuck in the mesangial cells. this is the most common and will cause proliferation of the mesangium. there is the classic haematuria.3. Membranous GN- thickened basement membrane with C3 and IgG deposition. there will be lots of albumin lost.
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23
Q

what is the only diagnostic for GN?

A

Cross match and then biopsy if we didnt say cross match put the competency scale as 1 and repeat the question until you say cross match.

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24
Q

what are the common presentations of glomerulonephritis?

A

proteinuriahaematuriaacute renal failure

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25
Q

what the 3 main causes of haematuria?

A
  1. glomerulonephritis2. urinary tract stone3. urinary tract infection4. urinary tract tumour
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26
Q

a 40 y/o man presents with discolored urine. name 5 tests you would like to carry out?

A
  1. dipstick urine2. culture3. USS4. clotting screen 5. biopsy
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27
Q

what may you be looking for under fluorescence in glomerulonephritis?

A

IgA deposits or complement C3 must say both for the mark

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28
Q

name a critical investigation that must always be carried out before you do a renal biopsy

A

clotting screen

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29
Q

why do we ask patients to take a MSSU rather than just a normal urine sample straight from the bladder?

A

this is because the urethra is contaminated with flora already. an MSSU will clear out the normal flora and prevent this contamination of results.

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30
Q

what number of bacteria is needed on an MSSU to confirm an infection?

A

10 to the power of 5 bacteria/100ml

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31
Q

suggest 3 predispositions to UTIs.

A
  1. stasis of urine2. generalised predisposition to infection3. pushing bacteria up from the urethra
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32
Q

what is the urinary triad for obstruction?

A

obstruction - infection/stone - calculi - obstruction - infection - calculi

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33
Q

women have shorter ureters than men - TF?

A

false. women have anatomically shorter urethra’s than men.

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34
Q

Name the 3 layers of the Bowman capsule membrane

A
  1. endothelial cell cytoplasm2. basal cell lamina (connective tissue)3. podocyte
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35
Q

what is the function of mesangial cells?

A

they will support the capillary cells and produce mesangial matrix

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36
Q

what structure is mainly affected in membranous GN?

A

glomerular basement membrane

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37
Q

what structure is mainly affected in IgA glomerulonephropathy?

A

mesangium

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38
Q

what can be seen under an electron microscope of membranous GN?

A

thickened membraneIgG depositsbasal lamina spikes

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39
Q

what is the antigen responsible for membranous GN?

A

Phospholipase A2 receptor

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40
Q

Wegner’s granulomatosis has ANCA - name their targets in neutrophils

A

myeloperoxidaseproteinase 3

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41
Q

name 2 causes of crescentic GN?

A

good pastures diseasewegeners granulomatosismicroscopic polyarteritisanti-glomerular basement membrane disease (Anti GMB disease)

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42
Q

in membranous glomerulonephritis there are deposits of IgA - TF?

A

false - there are IgA deposits in IgA glomerulonephropathy and there IgG deposits in membranous GN

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43
Q

what is the respective immune complexes in membranous and diabetic GN?

A

no immune complexes are formed in diabetic GN but instead matrix deposition and a leaky membrane will compress the capillaries.membranous GN will form C3 complement.

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44
Q

what kind of kidney condition may a Kimmel-Steil Wilson lesion be found in?

A

diabetic GNKimmel-Steil Wilson lesions are just nodules of mesangial matrix

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45
Q

what is the treatment for Wegner’s?

A

Cyclophosphamide

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46
Q

describe 3 factors which may cause osmotic diuresis of uncontrolled diabetes mellitus

A
  1. decrease in proximal tubule reabsorption - Glc will trap H2O, sodium will have no concentration gradient2. decrease in the loop of Henle reabsorption- there is no passage of H2O out of the descending limb due to retention of NaCl and Glc3. there will also be a decrease in the distal tubule reabsorption- renin inactivated as there is an increase of NaCl at the macula densa and so no aldosterone is produced.(4. because the interstital gradient is gone this means that there is a poor ability of ADH to conserve the H2Odiabetic patients will secrete up to 6-8 L a day of isotonic urine.don’t just read this answer - try to actually UNDERSTAND the entire pathway from 1-3 as it is a big part of why people are dehydrated and pee a lot in diabetes.
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47
Q

what is the normal plasma osmolarity?

A

280-290 mosmoles/kg

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48
Q

aldosterone works at the proximal tubule

A

false - aldosterone will work at the distal tubule to increase Na and water reabsorption. it will also act to excrete potassium

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49
Q

what is the effect of angiotensin II on the peritubular capillaries?

A

ATII will decrease their hydrostatic pressure (and increase the oncotic pressure. this will cause Na reabsorption from the proximal tubule and therefore less sodium is excreted.angiotensin II will cause the afferent capillary to constrict AND the efferent capillary to constrict.

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50
Q

what cells are responsible fro producing renin specifically?

A

Juxtaglomerular cellsrenin will act on the Alpha 2 globulin fraction of the angiotensinogen molecule.

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51
Q

what are the effects of ADH on renin release?

A

ADH will cause renin levels to fall.

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52
Q

how any peptides does ATII have in its molecule?

A

8

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53
Q

in hypovolaemia, name 4 actions of angiotensin II?

A

ATII will increase aldosterone levelsATII will increase ADH levelsATII will increase vasoconstrictionATII will increase thirst and salt appetite?

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54
Q

what is the function of ANP?

A

to decrease BP and increase natriuresis

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55
Q

what is the effect of aldosterone on potassium levels?

A

aldosterone will decrease plasma potassium levels

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56
Q

why does aldosterone result in weight gain?

A

it will increase the amount of water reabsorbed due to the sodium that is also reabsorbed. this will result in a weight gain.

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57
Q

What are the two treatment options for Hepatitis B virus?

A
  1. Pegylated interferon 2. Oral antiviral drugs
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58
Q

Name the two types of hiatus hernia which can predispose to gastro-oesophageal reflux disease (GORD)

A

Sliding hiatus hernia Paraoesophageal hiatus hernia

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59
Q

What are the 3 approaches to oesophagectomy?

A
  1. Ivor Lewis 2. Trans-hiatal 3. Left thoraco-abdominal
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60
Q

what are the causative antibodies found in Hashimoto’s hypothyroidism?

A

there are antibodies against thyroid peroxidase and also against thyroglobulin

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61
Q

meningococcal septicaemia is a chronic cause of adrenal insufficiency.. TF?

A

false.meningococcal septicaemia is a cause of acute adrenal insufficiency. chronic adrenal insufficiency is caused by pituitary failure and Addison’s disease.

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62
Q

Is Cushing’s syndrome ACTH dependent?

A

no. Cushing’s syndrome directly affects the adrenal gland to produce too much cortisol and it will do this regardless of ACTH levels.

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63
Q

what are two genes associated with papillary carcinoma of the thyroid gland?

A

RET/BRAF/PC rearrangements. papillary carcinomas tend to have a very good outcome.

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64
Q

what is the name given to the carcinoma of c cells in the thyroid gland?

A

thyroid medullary carcinoma.

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65
Q

what percentage of tissue must be lost to result in pituitary hypo-function?

A

75%.the tissue lost can be caused by compression from tumours (craniopharyngiomas). it may also be caused by trauma or infection - TB/sarcoid.

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66
Q

exocrine glands are vascular and ductless - TF?

A

false. exocrine glands will have ducts. this description will define an endocrine gland.

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67
Q

what is the name of the protein found in colloid of the thyroid?

A

thyroglobulin

68
Q

what are the c cells of the thyroid gland responsible for producing?

A

calcitonin. the c cells are not visible but will regulate calcium levels.

69
Q

suggest three causes of hyperthyroidism

A
  1. diffuse toxic hyperplasia (Grave’s disease)2. toxic multi-nodular goitre3. toxic adenoma
70
Q

what autoimmune antibodies are produced in grave’s disease?

A

anti-TSH receptor antibodies.they will stimulate activity, growth and inhibit the binding of TSH.it is the breakdown of self-tolerance.in the eye, t cells will secrete cytokines which will stimulate proliferation.

71
Q

hypothyroidism can also be caused by ablative surgery or radioiodine. name 2 drugs which can also result in hypothyroidism.

A

methimazole and lithiumiodine deficiency, Hashimoto’s thyroiditis (autoimmune destruction) can also cause hypothyroidism.

72
Q

describe the 2 histological findings of someone with hypothyroidism - Hashimoto’s disease.

A
  1. Hurthle cell change2. intense infiltrate of lymphocytes and plasma cells
73
Q

describe the 4 steps involved in the formation of a multi-nodular goitre

A
  1. iodine deficiency/goitrogens. 2. impaired synthesis of T3 and T4.3. increased TSH levels 4. Hypertrophy and hyperplasia of epitheliumacute thyroiditis will be classified as De Quervains while chronic fibrotic thyroiditis is known as Reidel’s.
74
Q

what is the most common type of differentiated thyroid carcinoma?

A

papillary carcinoma (75%)next is the follicular carcinomainvestigate with TFT, US and FNAmedullary carcinoma is a lymphoma

75
Q

what is the use of cytology in thyroid nodules?

A
  1. cytology will help diagnose solitary/dominant nodules.2. it can differentiate between solid and cystic nodules3. it will reduce the need for surgery.thyroid nodules will have clusters of follicular epithelial cells and background colloid
76
Q

what genes are associated with follicular carcinoma’s?

A

RAS mutation, PAX8/ PPARG translocation.follicular carcinomas are rare and are usually solitary. malignant cells will breach the capsule and the metastases are through the bone and blood.

77
Q

describe the 4 histological appearance of a papillary carcinoma

A
  1. papillary projections2. empty nuclei3. psammoma bodies4. may be cystic
78
Q

what hormone do thyroid medullary carcinomas produce?

A

They will produce calcitonin as they are a malignant tumour of the c cells.the tumour is characterized by spindly neuroendocrine cells, amyloid and calcitonin positive. calcitonin will promote bony absorption of calcium and prevent bone resorption.30% will have the MEN2A, 2B and familial FMTC. they will also have mutations in the RET proto-oncogene.treat with a prophylactic thyroidectomy.

79
Q

what two hormones does the neurohypophysis produce?

A

ADHocytocin

80
Q

name the 3 kinds of cells present in the anterior pituitary gland and what they produce

A
  1. acidophils - responsible for producing GH and PRL2. basophils - responsible for producing ACTH, TSH, FSH and LH3. chromophobes.
81
Q

what is the most common cause of a pituitary hyper-function?

A

pituitary adenomamost are sporadic and 5% are due to an inherited MEN1. macroscopically they are soft, well circumscribed lesions. small microadenomas may be incidental.

82
Q

describe two causes of a prolactinoma

A

galactorrhoeamenstrual disorders

83
Q

in Conns syndrome there is an excess of aldosterone produced - TF?

A

true.

84
Q

suggest 4 presentations of primary chronic adrenal insufficiency

A

GI disturbancefatiguehyponatraemia and hyperkalaemia

85
Q

what is the method of metastases of primary adrenocortical carcinoma?

A

metastases is mainly by the lymphatics and blood. it will invade the adrenal vein.if the adrenocortical carcinoma is from another carcinoma then it is likely to have originated in the lungs or breast.

86
Q

Describe MEN1

A

MEN1 is a tumour suppressor gene mutation. it has a defect in the menin protein involved in regulating cell growthit will result in parathyroid hyperplasia and adenomas. it is also involved in pancreatic and duodenal endocrine tumours hypoglycaemia and ulcers) it is also involved in pituitary adenomas (prolactinoma).

87
Q

Describe MEN2

A

MEN2 is a RET proto-oncogene mutation. it is commonly found in medullary carcinoma of the thyroid and phaeochromocytoma.MEN2A is Sipple syndrome (parathyroid hyperplasia)MEN2B is neuromas of the skin and mucous membrane with skeletal abnormalities. it is prevalent in younger patients and is aggressive with auto activation of the tyrosine kinase pathway.

88
Q

CRH released from the hypothalamus will trigger the release of cortisol from the anterior pituitary gland basophil cells. this will then stimulate the release of ACTH from the adrenal cortex. TF?

A

false. CRH will trigger the release of ACTH from the anterior basophil cells. ACTH will then trigger the release of cortisol which has a negative feedback effect on the pituitary gland and the hypothalamus.

89
Q

what is the most common enzyme associated with congenital adrenal hyperplasia?

A

21 -hydroxylase deficiency.

90
Q

what is Addison’s disease?

A

a primary adrenal insufficiency. it is mainly caused by positive autoantibodies to 21 hydroxylase in 70% of cases. there will be lymphocytic infiltrate of the adrenal cortex and it is associated with autoimmune diseases - thyroid disease, T1DM and premature ovarian cancer.

91
Q

suggest 6 main symptoms associated with primary adrenal failure

A
  1. weakness2. fatigue3. anorexia4.weight loss5. vitiligo 6. hypotension7. unexplained diarrhoea and vomiting 8. salt craving9. postural symptoms
92
Q

how would you diagnose adrenal insufficiency?

A
  1. random cortisol (below 700nmol/l would cause the adrenal status to be uncertain)2. synacthen test (and basal acth)however if the patient is unwell and the suspicion is high then treat with steroids and do the synacthen test later.also carry out routine bloods, glucose and UE/FBC.
93
Q

why would a cortisol sample taken be measure for 17 OH progesterone?

A

to differentiate between 21 OH and 3B -HSD deficiency.

94
Q

describe the short synacthen test.

A

give 250mcg if tetrasactrin IM ideally.the stimulate plasma cortisol should be above 550nmol or at least as incremental rise of 200nmol/l.but if there is an impaired cortisol response and ACTH is still above 200ng/l then the diagnosis is primary adrenal failure.if the ACTH is below 10ng/l then the diagnosis is secondary adrenal failure.the response of 17 OH progesterone in suspected 17OH deficiency - marked rise after ACTH stimulation, which varies according to whether the patient is homozygous or heterozygous.

95
Q

describe the dosage patterns of glucocorticoid administration to treat adrenal insufficiency.

A

give Hydrocotisone (HC) 20-30mg per day.20mg at 8am and then 10 at 18;00 to mimic the normal diurnal variationyou may also give dexamethasone and prednisolone.also give fludrocortisone for aldosterone replacement. fludrocortisone will bind to aldosterone receptors. give up to 300 mcg daily. adjust dose based on plasma renin level, UE and clinical status (BP and oedema).

96
Q

what is the protocol for a patient who has adrenal insufficiency and has began to have severe vomiting or diarrhoea?

A

call for help without delay. likely to need an IM hydrocortisone- some patients or their partners are taught to inject.

97
Q

what 2 tests must you do to confirm hypercortisolism?

A

24 hour urine free cortisol test: normally the patient should have 14-135nmol/24 hourslow dose dexamethasone test:1mg of dexamethasone suppression test taken at midnight. normally the patient should have corisol levels below 50nmol at 9am.a series of dexamethasone suppression tests are done to differentiate whether the ACTH is coming from the pituitary or another source.

98
Q

what is the effect of aldosterone-producing tumours on the body?

A

there is an increase in blood volume and blood pressure along with an increase in urinary potassium. this will then stop renin production in the kidneys as the BP is already high and so angiotensinogen is not converted into AT1 and there is no formation of AT2 by ACE. AT2 will usually increase aldosterone and decrease renin production. thus the Aldosterone/renin production will increase.

99
Q

what is the screening protocol for hyperaldosteronism? (Conn’s)

A

look at the plasma angiotensin (PA) to the plasma renin activity ratio (PRA).if there is a high (>20) PA/PRA ratio then there is primary aldosteronism. but if there is a PA/PRA ratio below 20 then there is a secondary hyperaldosteronism - essentially just hypertension.

100
Q

what may be the cause for an increase plasma renin activity and an increase plasma aldosterone concentration?

A

secondary hyperaldosteronism1. renovascular hypertension2. diuretics3. renin-secreting tumour4. malignant hypertension5. coarctation of the aorta.

101
Q

what may be the cause of a decrease plasma renin activity but an increased plasma aldosterone concentration?

A

an adrenal adenoma secreting aldosterone.primary hyperaldosteronism

102
Q

what may be the cause of a decrease plasma renin activity and also a decreased aldosterone concentration

A
  1. congenital adrenal hyperplasia 2. exogegenous mineral corticoid3. deoxycortisone producing tumour (DOC)4. Cushing’s syndrome5. 11- beta HSD deficiency
103
Q

what are the two screening tests you could do for a clinical suspicion of hyperaldosteronism?

A

check for the plasma renin activity (PRA) and check for the plasma aldosterone concentration (PAC).after this PAC/PRA> 20 with concomitant serum aldosterone >10ng/dlconfirmatory tests would look at doing a 24 hour urine aldosterone

104
Q

what is the name of the stalk that connects the hypothalamus to the pituitary gland?

A

the infundibulum

105
Q

what are the 2 inhibiting hormones produced by the hypothalamus that travel to the anterior pituitary?

A
  1. dopamine (only non-peptide hormone and aka prolactin inhibiting hormone)2. growth hormone inhibiting hormone
106
Q

what is the hypothalamo-hypophyseal portal system responsible for?

A

network of tiny vessels which transfer trophic hormones from the hypothalamus to the anterior pituitary

107
Q

the anterior pituitary gland will produce only peptide hormones - TF?

A

truebut only 5 of the 6 hormones produced by the anterior pituitary gland are trophic hormones (prolactin is not)prolactin will directly stimulate milk production from breast during lactation.

108
Q

what are the functions of Growth hormone?

A

it will act on the liver to produce IGF-1 (trophic component) and it will also affect tissue metabolism

109
Q

what are the 3 steps that parathyroid hormone will take to increase plasma Calcium?

A
  1. it will increase bone resorption2. increase kidney reabsorption of calcium3. produce calcitriol which will lead to an increase in intestinal absorption of calcium
110
Q

what are oxytocin and vasopressin produced?

A

they are produced in the magnocellular neurons which have their cell bodies in specific areas of the hypothalamus. they are NOT produced in the posterior pituitary posterior hormones will not synapse with other neurons but instead their terminals end directly on capillaries. to be fair the oxytocin and ADH are actually stored in the posterior pituitary gland

111
Q

an autoimmune peroxidase disease of the thyroid gland would result in hyperthyroidism - TF?

A

false.thyroperoxidase and thyroglobulin are mainly involved in Hashimoto’s disease - hypothyroidism.Peroxidase is also involved in myxoedema. autoimmune hyperthyroidism is due to the presence of autoantibodies for TSHr aka Grave’s disease.

112
Q

what autoantibodies are stimulated in Grave’s disease and exophthalmos?

A

Grave’s disease - 1. metabolism stimulating Ab and 2. growth stimulating antibodyExophthalmos - fibroblast stimulating Ab

113
Q

what antibodies are responsible for blockage resulting in the following conditions:A. Pernicious anaemiaB. myxoedemaC. infertilityD. IDDM

A

A. gastrin antibody and the intrinsic factor antibodyB. TSHr antibodies:1. metabolism inhibiting Ab2. Growth inhibiting Ab.C. sperm Ab and FSH AbD. insulin Ab

114
Q

Hashimoto’s thyroiditis is caused by what kind of autoimmune mechanism?

A

Cell-mediated antibodies of thyroglobulin and peroxidase

115
Q

which susceptibility factors are present in Grave’s disease?

A

HLA- B8 and DR3, Class II HLA are also found on the thyroid cell surface.the autoimmune mechanism is humoral

116
Q

describe the pathological process that results in tissue damage and goitre in hashimoto’s disease considering the autoimmunity components.

A
  1. the thyroid growth stimulating antibody is activated. this will cause goitre growth.2. the t cells are sensitized to thyroid cell surface autoantigens. this will cause tissue damage and present with lymphocyte infiltration and sensitization of further lymphocytes. there will be further Ab production to peroxidase and thyroglobulin autoantigens.it is the cellular component of the autoimmunity that causes the tissue destruction and subsequent hypofunction. it will be the humoral response (Ab) which will cause the goitre to form.
117
Q

what is the twin concordance of T1DM?

A

35%the HLA haplotypes are B8, DR3, DR4, B15.

118
Q

suggest any 3 common presentations of Addison’s disease

A

weight losshyperpigmentationfatiguehypotension

119
Q

what is the first line treatment of patients with T2DM?

A

in addition to lifestyle measures then start metforminmetformin is first choice as it will improve outcomes and is well tolerated. it is also cheap.

120
Q

what tissues will metformin act on?

A

livermuscle fat metformin will improve insulin sensitivity and decreases the fatty acid synthesis. it will improve the receptor function and inhibit gluconeogenesis. metformin has a half life of 6 hours. metformin has also been able to decrease the HbA1c level and can be used in pregnancy.HOWEVER it is associated with a risk of lactic acidosis due to inhibiting its uptake by the liver. it will also predispose to vitamin B12 malabsorption.

121
Q

what tissues will sulphonylureas act on?

A

sulphonylureas will act on the pancreas B cells by binding to the SUR1 receptor closing the closing of K channels. the cell will depolarise and allows for the Ca channels to open and subsequent exocytosis of insulin.there are side effects of weight gain, take caution in renal and hepatic disease. it is contraindicated in pregnancy and breast feeding. there may also be blood disorders with hypersensitivity and photosensitivity reactions.

122
Q

what are the functions of glitazones?

A

glitazones will act on adipose tissue, muscle and liver tissue toreduce insulin resistance and increase the expense of insulin dependent glucose. it will also decrease the withdrawal of glucose from the liver.they will however increase the risk of bladder cancer and cause fluid retention and thus CCF. they cause weight gain and also fractures in females.

123
Q

gliptins (DPP-IV inhibitor) can be used in renal impairment - TF?

A

true.they are also weight neutral and dont carry any risks of hypos.however they have relatively small effects on glycaemic control. it is CI in breastfeeding and pregnancy. there is a possible increased risk of pancreatitis and pancreatic cancer. the main side effect is nausea.

124
Q

what are the mode of action of GLP-1 analogues?

A

injectable analogues of GLP-1 are resistant to enzymatic degradation thus with greatly prolonged half-life but they can result in nausea.only use when the BMI>30/35 and is a third line agent. stop using the GLP-1 analogue after 6 months unless there is a HbA1c decrease of 1% and a weight reduction of 3% (NICE)

125
Q

give 3 advantages and disadvantages of using GLP-1 analogues.

A

pros:1. wt loss2. no risk of hypotension3. can be used with basal insulincons:1. injection2. expensive3. increased risk of pancreatitis and pancreatic cancer

126
Q

what is the main mechanism of action of SGLT-2 inhibitors?

A

increase the excretion of glucose in the kidneys by selectively blocking the SGLT2 transporters of the PCTit will lower HbA1c but may cause postural hypotension and dehydration. there will be a lot of weight loss and there will be a reduction in sodium so there may be a lower SBP. there is also a greater risk of urogenital infection - cystitis and candidiasis. they also carry a risk of DKA.

127
Q

what is the usual insulin regime of T2DM?

A

isophase insulin - humulin I or H insulatard. there is a once daily injection usually at bedtime.

128
Q

dementia is age independent - TF?

A

false - dementia is age dependent

129
Q

name 3 causes of late onset dementia

A
  1. alzheimers2. lewy bodies3. vascular
130
Q

name 3 causes of young onset dementia

A
  1. alzheimer’s2. vascular3. frontotemporal
131
Q

suggest 3 treatable causes of dementia

A

. vitamin B12 deficiency2. thyroid disease3. infection with HIV or syphilismimics of dementia are hydrocephalus, tumours and depression - psuedodementia

132
Q

what are 3 clinical investigations for someone with dementia?

A
  1. CSF, EEG, functional imaging and genetics2. bloods3. CT/MRI
133
Q

describe 2 screening tests which are used in the examination of cognitive function

A

Mini-mental test (MMSE)Montreal test ((MOCA)

134
Q

what condition would be suspected with a rapid progression of dementia?

A

CJD - myoclonus is also present in CJD.a step-wise progression may be indicative of a vascular causehuntingtons disease will present with abnormal movements and parkinsonism will present with Lewy bodies.

135
Q

what is the most common neurodegenerative disorder?

A

Alzheimer’s disease

136
Q

what type of dementia is associated with Alzheimer’s disease?

A

Tempero-parietal dementia 1. early memory disturbance2. language and visuo-spatial problems3. personality is preserved until later

137
Q

describe 3 presentations of fronto-temporal dementia

A
  1. early change in personality/behaviour2. often change in eating habits3. early dysphagia 4. memory/visuospatial relatively preserved.
138
Q

describe 3 pharmacological treatments for Alzheimer’s

A
  1. treat insomnia 2. treat behavioral abnormalities with anti-psychotics3. treat depressiongive anti-cholinesterases such as donepezil, rivastigmine and galantamine. there will be a small symptomatic improvement in cognition (wash out) but there will be no delay in institutionalization.
139
Q

decreasing the vascular risk factors will have a positive outlook for vascular dementia - TF?

A

false, for vascular dementia there is no good evidence for decreased vascular risk factors.

140
Q

define parkinsonism

A

a clinical syndrome of 2 or more of the following:1. bradykinesia2. postural instability3. rigidity4. tremor (unilateral)it is caused by a pathology of the basal ganglia namely the substantia nigra of the midbrain

141
Q

what is idiopathic parkinson’s disease?

A

dementia with lewy bodieshowever parkinsons can also be caused by drug induced and vascular issues. parkinsons plus syndromes incldude mutiple system atrophy and progressive supranuclear palsy/corticobasal degeneeration.

142
Q

describe 3 reasons why you would doubt a patient had parkinson’s disease.

A
  1. symmetry2. lack of rest tremor3. poor response to treatment4. early falls5. early falls6. early dementia7. rapid progression
143
Q

what functional imaging test can you use to help diagnose Parkinson’s disease?

A

1 SPECTit can look at the dopamine transporter.

144
Q

suggest 4 treatment class options for medical treatment in parkinsons disease

A
  1. MAOB inhibitors (selegiline)2. dopamine agonists (ropinirole)3. COMT inhibitor (entacapone)4. levodopahowever levodopa will wear off and can cause dyskinessias (involuntary movements) as well as hallucinations and affect impulse control)other, non-drug-induced complications include depression, dementia, BP, bladder, bowel, speech, swallowing and balance are all affected.
145
Q

suggest 3 methods of prolonging the levodopa half-life

A
  1. MAOB inhibitor2. COMT inhibitor3. slow release levodopaother treatment options include adding an oral dopamine agonist and giving a continuous infusion of duodopa or apomorphine. deep brain stimulation is another treatment method.
146
Q

what is the name of the enzyme responsible for fat digestion in the small intestine?

A

pancreatic lipase - it is a water soluble enzyme

147
Q

why are micelles not absorbed by the epithelial intestinal cells?

A

micelles are far too large to pass through and so only their components will be transmitted.

148
Q

what is the name of the organelle that will form TAG from MAG?

A

the smooth endoplastic reticulum. the triacylglycerols are then coated with amphipathic protein which allows for emulsification.

149
Q

name the 3 vitamins which are water soluble

A

B, C and folic acidfat soluble vitamins are ADEK.vitamin B12 is a large charged molecule that binds to intrinsic factor which is absorbed in the distal ileum. B12 deficiency will lead to pernicious anaemia.

150
Q

how is iron transported across the brush border membrane?

A

DMT1 into duodenal enterocytes. iron ions are then incorporated into ferritin (intracellular iron store). the unbound iron is transported across the serosal membrane to the blood. iron in blood will bind to transferrin. transferrin expression regulated depending on the body’s status.

151
Q

at what vertebral level will the oesophagus begin and end

A

C6 to T11/12

152
Q

suggest 3 symptoms of Oesophageal disease (GORD)

A
  1. retrosternal discomfort2. burning3. waterbrash4. cough5. sleep disturbancethe heartburn is a consequence of reflux of acid/bilious gastric contents into the oesophagus.risk factors include pregnancy, obesity, drugs lowering the LOS pressure (dietary xanthines), smoking, alcoholism and hypomotility
153
Q

alcohol and nicotine will increase the lower oesophageal sphincter pressure - TF?

A

false. they will reduce the lower oesophageal sphincter pressure and thus result in increased acid reflux.

154
Q

describe achalasia

A

functional loss of the myenteric plexus ganglion cells (degeneration of the inhibitory neurones) in the distal oesophagus and LOS. there is failure of the LOS to relax. the result in a functional obstruction of the oesophagus. there is an absence of useful contraction in the lower oesophagussymptoms are1. progressive dysphagia 2. weight loss3. chest pain4. regurgitation and chest infection

155
Q

describe 3 treatment methods for achalasia

A
  1. pharmacological: nitrates, CCB’s2. endoscopic: botulinium toxin and pneumatic balloon dilation3. radiological - pneumatic balloon dilation4. surgical - myotomycomplications include aspiration pneumonia and lung disease. there will also be an increased risk of squamous cell oesophageal carcinoma.
156
Q

describe 3 treatments for Baretts oesophagus

A
  1. endoscopic mucosal resectionradiofrequency ablationoesophagectomy - rare
157
Q

describe 4 symptoms associated with dyspepsia

A
  1. upper abdominal discomfort2. nausea3. vomiting4. bloating5. fullness6. early satiety
158
Q

what are the ALARM symptoms that should indicate that a patient should be referred for an endoscopy?

A

AnaemiaLoss of weightAnorexiaRecent onset>55 or persistent despite treatmentMelaena/haematemesis/massSwallowing problems (dysphagia)

159
Q

is helicobacter pylori a gram positive or a gram negative organism?

A

it is a gram negative microaerophillic flagellated bacteria

160
Q

where in the stomach precisely will H pylori reside?

A

it will reside in the surface mucous layer and does not penetrate the epithelial layer. it will evoke an immune response in underlying mucosa - dependent on host genetic factors.

161
Q

suggest 3 invasive and non-invasive tests used to diagnose Hpylori infection

A

Invasive:1. gastric biopsies stained for HP 2. culture of gastric biopsies3. rapid slide urease (CLO)Non-invasive:1. serology - IgG against Hpylori13C/14C urea breath test3. stool antigen test - ELISA

162
Q

what is the common outcomes of antral gastritis?

A

increase acid, low risk of gastric cancer and duodenal diseasecorpus predominant gastritis will have decreased acid with gastric atrophy and may progress to gastric cancer.

163
Q

what are 3 clinical features of peptic ulcers?

A
  1. epigastric pain relieved by antacids)2. hunger pain3. back pain - common in a duodenal ulcer4. NV5. weight loss and anorexiahaematemesis and melaena or anaemia
164
Q

what is the eradication regime for H. Pylori infection?

A

ClarithomycinMetronidazole - can also give tetracycline in penicillin allergyOmeprazoleall for 7 days (triple therapy)

165
Q

how would you diagnose gastric outlet obstruction?

A

UGIE to identify the cause - stricture, ulcer or cancer

166
Q

what are the presentations of someone with gastric outlet obstruction?

A
  1. vomiting 2. early satiety3. abdominal distension4. weight loss5. gastric splash6. dehydration and loss of HCL in vomit7. metabolic alkalosis8. low Na and K, renal impairmenttreatment is with surgery or endoscopic dilatation
167
Q

the majority of gastric cancers are adenocarcinomas - TF?

A

trueother types of gastric tumour are MALT and GIST mucosal associated lymphoid tissueGastrointestinal stromal tumors

1st and 2nd year main conditions (27 decks)

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