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endocrine, derm + misc Flashcards

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1
Q

what is the pathology of acne

A
  • blocked hair follicles
  • sebum from sebaceous glands increases
  • excess mixed with dead skin cells and forms a plug in follicle
  • if plug close to surface = white head
  • if open to skin = black head
  • sebum stagnated when blocked in by narrowed hair follicle (No oxygen)
  • p.acnes breakdown triglycerides causing irritation and inflammation
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2
Q

what are the causes of acne

A
  • increased testosterone during puberty - causes increased sebum
  • acne in families
  • in women - hormones during pregnancy, periods and PCOS
  • cosmetics
  • medications e.g steroids
  • smoking
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3
Q

describe the grading of acne

A
    1. mild - whiteheads and blackheads mostly
      1. moderate - multiple pustules and papules - mostly on face
      2. moderately severe - a large number of papules and pustules, occasional inflamed nodule - back and chest also
      3. severe - large painful pustules and nodules
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4
Q

what is the treatment of acne

A
  • topical retinoids - exfoliate dead cells
  • topical antibiotics
  • azelaic acid
  • combined OC
  • isotretinoin tablets - decrease sebum, bacteria and swelling
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5
Q

what is the pathology of eczema

A

genetics

  • FLG - filaggrin - loss of functional variants of epidermal barrier - increased PH, increased protease activity (due to decreased natural moisturising factor which maintains acid environment outside of cell)
  • KLK7 genetic variants - proteases increase
  • increased protease activity causes accelerated desquamation
  • inhibited lipid lamellae synthesis
  • water out
  • allergens in
  • TH1 bacterial response
  • TH2 immune response producing IgE

environment

  • soap and detergents
  • house dust mite
  • hard water
  • colonisation and infection
  • topical products
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6
Q

what are the symptoms of eczema

A
  • itchy
  • dry
  • red
  • cracked
  • sore
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7
Q

what is the treatment of eczema

A
  • avoid all soap and detergents
  • use emollient soap substitutes
  • use emollient bath oils
  • use emollient shower products
  • shampoos should only contain very mild surfactand formulations
  • emollient cream 3-4 times per day

stages

  1. complete emollient therapy
  2. identification and avoidance of allergens/triggers
  3. treatment and prevention of flare ups with TCI and TCS
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8
Q

what are the complications of erthyrodermal psoriasis

A
  • disturbed thermoregulation
  • H20 loss
  • protein loss
  • CV strain
  • malabsorption
  • decreased Ca2+
  • decreased uric acid
  • folate deficiency
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9
Q

list some different types of psoriasis

A
  • guttate - small lesions over upper trunk and proximal extremities
  • scalp
  • nail
  • flexural
  • napkin
  • erthyroderma - widespread reddening
  • pustular
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10
Q

what is the pathology of psoriasis

A
  • increased production of skin cells - every 3-7 days as apposed to 3-4 weeks
  • genetics are involved
  • triggered by injury to skin, throat infections, using certain medications
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11
Q

what is the treatment of psoriasis

A
  1. emollients
  2. TCS
  3. phototherapy
  4. systemic
  • vitamin D analogues - calcipotriol
  • tar
  • clithranol
  • UVB- TLOI
  • PUVA

Systemic

  • methotrexate
  • ciclosporin
  • hydroxyurea
  • vit A analogues
  • anti TNFa
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12
Q

describe the features of malignant melanoma

A
  • younger pts
  • early diagnosis vital
  • change in size, shape, colour of mole
  • inflammation, sensory change, diameter >7mm
  • crusting or bleeding
  • urgent excision and chemo in metastases
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13
Q

describe squamous cell carcinomas

A
  • usually presents as an ulceration lesion with hard, raised edges, in sun exposed sites
  • excision and RT
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14
Q

describe basal cell carcinomas

A
  • typically a pearly nodule with rolled edge
  • on face or sun exposed site
  • excision
  • cryotherapy
  • topical flurouracil
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15
Q

what are the causes of skin ulcers

A
  • arterial disease (70%)
  • arterial and venous mixed
  • venous
  • vasculitis
  • infection (TB, syphilis)
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16
Q

what is the management of skin ulcers

A
  • of underlying cause
  • focus on prevention
  • dressings
  • surgery and larval therapy
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17
Q

why may a pt be at risk of cellulitis

A
  • poor circulation
  • find it difficult to move around
  • immunosuppressed
  • bed sores
  • lymphoedema
  • IVDU
  • surgery wound
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18
Q

what is the management of cellulitis

A
  • antibiotics - flucloxacillin for s.aureus, Benpen for strep pyogenes
  • pain relief
  • raise area
  • regularly move joint
  • drink plenty of fluids
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19
Q

what are the complications of cellulitis/when should pt go to A&E

A
  • temperature
  • tachycardia
  • purple patches
  • cold clammy skin
  • dizziness
  • confusion
  • unresponsiveness
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20
Q

what is necrotising fascutis

A
  • flesh eating disease

- bacteria release toxins that damage nearby tissue

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21
Q

what are the symptoms of necrotising fascutis

A
  • small cut
  • intense pain
  • temperature
    then
  • swelling and redness
  • D+V
  • dark blotches on skin that turn into fluid filled blisters
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22
Q

what is the management of necrotising fascutis

A
  • surgery to remove infected tissue
  • antibiotics
  • supportive treatment
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23
Q

what are the causes of necrotising fascutis

A
  • cuts and scratches
  • insect bites
  • puncture wounds from IVDU
  • surgical wounds
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24
Q

what is acromegaly

A

-increasing size of bones including hands, feet and face

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25
what is the pathology of acromegaly
- increased secretion of GH from a pituitary tumour (99%) or hyperplasia - GH stimulates bone and soft tissue growth through increased secretion of insulin like growth factor (IGF-1) - 5% associated with MEN1 - incidence UK 3million/year - mean age diagnosis 44
26
what are the symptoms and signs of acromegaly
- acroparaesthesia - (burning, tingling, numbness of extremities) - amenorrhoea (missing periods) - decreased libido - headache - sweating - snoring - arthralgia - backache signs - increased growth of hands, jaw and feet - coarsening of face, wide nose - big supraorbital ridges - macroglossia (big tongue) - widely spaced teeth - puffy lips, eyelids and skin - carpal tunnel
27
what are the complications of acromegaly
- impaired glucose tolerance and DM - hypertension and heart disease - cerebrovascular events and headaches - arthritis - sleep apnea - neoplasia
28
criteria for diagnosis of acromegaly (exclusion)
``` - random GH <0.4ng/ml and normal IGF1 if either abnormal proceed to - 75gm glucose tolerance test then exclude if -IGF1 normal and GTT nadir GH <1ng/ml ```
29
why are levels of GH unreliable in diagnosis of acromegaly
- random GH secretion is pulsatile and during peaks acromegalic and normal levels overlap - GH increases also in stress, sleep, puberty and pregnancy
30
what tests can be used to diagnose acromegaly
- Glucose tolerance test - Random GH (unreliable) - MRI of pituitary fossa - ECH, ECHO - old photos - visual field tests
31
what is the treatment of acromegaly
- aims to restore basal GH and IGF1 to normal levels - relief of symptoms - reversal of visual and soft tissue changes - prevention of further skeletal deformity - normalisation of pituitary function 1. Transpenoidal surgery is first line 2. somatostatin analogues (SSA) and/or RT e.g octreotide or lanreotide control GH and IGF1 3. GH antagonist pegvisomant suppresses IGF1 4. dopamine agonists
32
what is a prolactinoma
- lactotroph cell tumour of pituitary - 90 per 100000 - women >men
33
what are the features of prolactinoma
local tumour effect - headache - visual field defect - CSF leak - menstrual irregularity - infertility - galactorrhoea - milky nipple - low libido - low testosterone in men
34
how is prolactinoma managed
- dopamine agonists
35
what are the ways that a pituitary tumour can cause pathology
1. pressure on local structures e.g optic nerves - bitemporal hemianopia - headaches - cranial nerve palsies and temporal love epilepsy (Lateral projection) - cerebrospinal fluid rhinorrhoea ( inferior projection) 2. pressure on normal pituitary - hypopituitarism 3. functioning tumour - prolactioma (inc prolactin) - acromegaly (inc GH) - cushings disease (inc cortisol)
36
give examples of non functioning pituitary tumours
- craniopharyngioma - meningioma - non functioning pituitary adenoma
37
describe the pathology and symptoms of craniopharyngioma
- arise from squamous epithelial remnants of Rathkes pouch - either squamous papillary (well circumscribed) or adamantinous (cyst formation and calcification) - benign though infiltrates surrounding structures - inc ICP - visual disturbance - growth failure - hypopituitarism - increased weight - developmental abnormality
38
which hypothalamic hormone causes release of thyroid stimulating hormone (TSH) from the anterior pituitary
thyrotropin releasing hormone (TRH)
39
Gonadotrophic releasing hormone (GnRH) causes release of which hormones from the anterior pituitary
- follicular stimulating hormone (FSH) | - luteinizing hormone (LH)
40
dopamine (DA) released from the hypothalamus has what effect on the anterior pituitary
inhibits prolactin release
41
somatostatin released from hypothalamus causes what effect on anterior pituitary
inhibits release of GH
42
which hormone released from hypothalamus causes release of adrenocorticotrophic hormone (ACTH) from anterior pituitary
- corticotrophin releasing hormone (CRH)
43
what is ACTH's target organ and what does it cause
- adrenal cortex - releases cortisol
44
what is produced in the adrenal cortex/where
1. glucocorticoids (zona fasciculata) - regulate glucose metabolism e.g cortisol 2. mineralcorticoids ( zona glomerulosa) - regulate mineral balance e.g aldosterone 3. androgens (zona reticularis) e.g testosterone
45
what is cushings syndrome
the clinical state induced by chronic glucocorticoid excess and loss of normal feedback mechanisms of the hypothalamopituitary adrenal axis
46
what are the causes of cushings syndrome
1. ACTH dependent causes (increased ACTH) - Cushings disease - bilateral adrenal hyperplasia from an ACTH secreting pituitary adenoma - ectopic ACTH production - especially small cell lung cancer and carcinoid tumours 2. ACTH independent causes (decreased ACTH due to -ve feedback) - iatrogenic - pharmacological doses of steroids - adrenal adenoma - adrenal nodular hyperplasia commonest cause = steroid PO
47
what are the symptoms of cushings syndrome
- weight gain - mood change (depression, lethargy, irritibility, psychosis) - proximal weakness - gonadal dysfunction signs - moon face - striae - acne - buffalo hump - skin and muscle atrophy - hypertension - osteoporosis - infection prone
48
what are the tests for cushing's syndrome
- do not rely on random serum cortisol - or MRI as 70% of tumours causing cushings disease are too small to be detected by MRI - overnight dexamethasone suppression test - no suppression of cortisol in the morning in cushings syndrome - 48 hour dexamethasone suppression testing
49
what is the treatment of cushings syndrome
- iatrogenic - stop medications if possible - cushings disease - transpenoidal removal of pituitary adenoma - adrenal adenoma/carcinoma - adrenalectomy and RT - ectopic ACTH - surgery is tumour located and hasn't spread
50
what is addisons disease
- primary adrenal insufficiency | - destruction of adrenal cortex leads to glucocorticoid and mineralcorticoid deficiency
51
what is the cause of Addisons disease
- 80% autoimmune in UK - TB most common cause worldwide - adrenal metastases from lung, breast, renal - lymphoma - opportunistic in HIV - adrenal haemorrhage - congenital
52
what is the cause of secondary adrenal insufficiency
- hypopituitarism (lack of ACTH) - due to: - pituitary macroadenoma/craniopharyngioma - hypophysitis (pituitary inflammation - mets - infection - RT - congenital
53
what is the cause of tertiary adrenal insufficiency
- steroids suppressing pituitary axis
54
what are the symptoms of adrenal insufficiency
- fatigue - weightloss - adrenal crisis - headache - poor recovery from illness -vomiting and abdo pain signs - pigmentation and pallor - hypotension
55
what are the tests for adrenal insufficency
- Na+ decrease, K+ increase due to decreased mineralocorticoids - decreased glucose (due to decreased cortisol) - eosinophilia - anaemia - inc Ca2+ - inc TSH - cortisol >500 AI unlikely <100 likely - ACTH > 22 primary - ACTH <5 secondary - synacthen test (short ACTH stumulation test) - >500 cortisol after test = unlikley - 21hydroxylase adrenal autoantibodies +ve in AI disease in 80% - increased renin
56
what is the treatment of adrenal insufficiency
- hydrocortisone (pharmaceutical name for cortisol) 2-3x per day - aldosterone replacement w/ fludrocortisone (in primary)
57
what are the signs of adrenal crisis
- Decreased Na+ - increased K+ - decreased glucose - fever - fatigue - hypotension and CV collapse
58
what is the management of adrenal crisis
- bloods - immediate hydrocortisone IV, IM - fluids - hydrocortisone 50-100mg IV/IM 6 hourly - in primary start flucortisone 100-200mg - when pt stable wean to normal replacement
59
what is Conns syndrome
- excess production of aldosterone causing inc Na and water retention, and decreased renin release due to solitary aldosterone producing adenoma
60
what are the symptoms of hyperaldosteronism
- asymptomatic or of hypokalaemia: weakness, cramps, paraesthesiae, polyuria, hypertension
61
what are the causes of hyperaldosteronism
2/3 conn's syndrome | 1/3 due to bilateral adrenocortical hyperplasia
62
what are the tests for hyperaldosteronism
- U+E - renin and aldosterone - dont rely on hypokalaemia
63
what is the treatment of hyperaldosteronism
- Conn's - laproscopic adrenalectomy and spironolactone 4 weeks pre op - hyperplasia - spironolactone or amiloride
64
give an example of secondary hyperaldosteronism
- due to high renin from decreased renal perfusiong e.g renal artery stenosis, diuretics, hepatic failure
65
what are the symptoms and signs of thyrotoxicosis/hyperthyroidism
- diarrhoea - weight loss - appetite increase - overactive - sweats - heat intolerance - palpitations - tremor - irritibility - labile emotions - oligomenorrhoea - infrequent periods signs - tachycardia - warm moist skin - fine tremor - palmar erythema - thin hair - lid lag - lid retraction - goitre- palpable and visible thyroid enlargement - hyperreflexia - restlessness
66
what are the three mechanisms for thyrotoxicosis (increased thyroid hormones in blood)
a. overproduction of thyroid hormone (hyperthyroidism) b. leakage of preformed hormone from thyroid c. ingestion of excess thyroid hormone
67
what are the tests for thyrotoxicosis
- decreased TSH, increased T4 or T3 - mild normocytic anaemia - mild neutropenia - inc ESR, inc LFT, inc Ca2+ - check thyroid autoantibodies
68
what are the causes of thyrotoxicosis
- graves disease - toxic multinodular goitre - toxic adenoma
69
what is graves disease/ pathology
- 2/3 of cases of hyperthyroidism - female:male 9:1 - 40-60 - caused by circulating IgG autoantibodies binding to and activating G protein coupled thyrotropin receptors, which cause thyroid enlargement and increase hormone production Thyroid-stimulating immunoglobulin, antithyroglobulin antibodies, anti-thyroid peroxidase antibodies - HLA -DR3 associated - environmental - stress, increased iodine intake, smoking, infection, childbirth - associated w/ other AI diseases - vitiligo, addisons, type 1 DM
70
what is toxic multinodular goitre
- seen in elderly and iodine deficient areas | - nodules secrete thyroid hormones
71
what is toxic adenoma
- solitary nodule producing t3+t4 | - hot nodule on isotope scan and rest of gland suppressed
72
what is the treatment of thyrotoxicosis
1. drugs thionamines e.g carbimazole, PTU -decrease synthesis of new thyroid homrone - PTU inhibits T4-->T3 - titration regimen (12-18 months) - block and replace regimen with T4 (levothyroxine) 6-12 months SE: AGRANULOCYTOSIS- decreased neutrophils, manifests as sore throat, fever, mouth ulcers 2. Radioiodine - emits beta particles resulting in ionization of thyroid cells, causing direct damage to DNA and enzymes - most become hypothyroid after treatment 3. surgery - thyroidectomy for Graves MNG and adenoma
73
what are the symptoms and signs of hypothyroidism
- tiredness - sleepy - lethargic - decreased mood - cold disliking - weight gain - constipation - menorrhagia - hoarse voice - decreased memory/cognition - dementia - myalgia - cramps - weakness ``` signs Bradykardia Reflexes relax slowly Ataxia Dry thin hair Yawning Cold hands Ascites Round puffy face Defeated demeanor Immobile CCF ```
74
How is hypothyroid diagnosed
- inc TSH | - decreased T4
75
what are the causes of hypothyroidism
Primary AI - primary atrophic hypothyroidism (female: male 6:1) diffuse lymphocytic infiltration of the thyroid, leading to atrophy, therefore no goitre - Hashimotos thyroiditis - goitre due to lymphocytic and plasma cell infiltration primary other - iodine deficiency - post - thyroidecomy or radioiodine - drug induced secondary - not enough TSH due to hypopituitarism (decreased TSH and T4)
76
what is the treatment of hypothyroidism
- levothyroxine (T4) - in IHD start on lower dose as may precipitate angina or MI - T4 t1/2 = 7days so wait 4-6 weeks until check if dosing right
77
what are the signs and symptoms of hyperkalaemia
- fast irregular pulse - chest pain - weakness - palpitations
78
what will be found on an ECG for hyperkalaemia
- tall tented T waves - small P - wide QRS
79
what are the causes of hyperkalaemia
- oliguric renal failure - K+ sparing diuretics - Addisons disease - metabolic acidosis (DM) - drugs e.g ACE-I
80
what is the treatment for hyperkalaemia
non urgent - polystyrene sulfonate resin - binds K+ in gut preventing absorption urgent - calcium chloride + insulin (which stimulates intracellular K+ uptake)
81
what are the symptoms of hypokalaemia
- muscle weakness - hypotonia - hyporeflexia - cramps - tetany - constipation - palpitations
82
what is seen on an ECG when a pt has hypokalaemia
- small or inverted t waves - prominent U waves - long PR interval - depressed ST
83
what are the causes of hypokalaemia
- diuretics - vomiting and diarrhoea - cushings syndrome/steroids/ACTH - Conn's syndrome - alkalosis - pyloric stenosis
84
what is the treatment of hypokalaemia
- K+ supplements
85
what are the signs and symptoms of hypercalcaemia
- abdo pain - vomiting - constipation - renal stones - CA - hypertension - tiredness - confusion
86
what is seen on an ECG when a pt has hypercalcaemia
- decreased QT interval
87
what are the causes of hypercalcaemia
- maligancy - primary hyperparathyroidism - vit d intoxication - thyrotoxicosis
88
what is the treatment of hypercalcaemia
bisphosphonates e.g alendronate
89
what are the symptoms of hypocalcaemia
- cramps | - paraesthesia
90
what is seen on an ECG when a pt has hypocalcaemia
- INCREASED QT
91
what are the causes of hypocalcaemia
- Vit D deficiency - osteomalacia - kidney disease - hypoparathyroidism
92
what is the treatment of hypocalcemia
calcium supplementation | - calcium gluconate
93
what are the symptoms + treatment of hypernatraemia
- lethargy - thirst - weakness - confusion treatment H20!
94
what are the causes of hypernatraemia
- fluid loss without replacement | - diabetes insipidus
95
what is diabetes insipidus/pathology
- passage of large volumes of dilute urine due to impaired water resorption by the kidney - due to decreased ADH secretion from posterior pituitary (cranial DI) or impaired response of kidneys to ADH ( nephrogenic DI)
96
what are the symptoms of DI
- polyuria (large volumes of urine) - of hypernatraemia - dehydration - polydipsia
97
what are the causes of DI
nephrogenic - inherited - drugs - CKD - metabolic (decreased K+, increased Ca2+) cranial - idiopathic - congenital - tumour e.g craniopharyngioma - AI hypophysitis - haemorrhage - hypophysectomy
98
what is the treatment of DI
cranial - MRI (head) - test ant pituitary function - give desmopressin (synthetic analogue of ADH) nephrogenic - treat cause - bendoflumethiazide - NSAIDs inhibit prostaglandin synthase ---> PG's locally inhibit ADH
99
what are the signs and symptoms of hyponatraemia
- anorexia - nausea - malaise - headache - irritibility - confusion - weakness
100
what are the causes of hyponatraemia
dehydration - Na+ and H20 loss via kidneys e.g Addisons disease, renal failure, diuretic excess - Na+ and H20 lost in way other than kidneys e.g D+V, fistulae, burns, SBO, CF, trauma ``` not dehydrated oedematous - nephrotic syndrome - cardiac failure -liver failure - renal failure non oedematous - SIADH -water overload -hypothyroid ```
101
how is syndrome of innappropriate ADH secretion diagnosed
- concentrated urine (Na+ > 20mmol/L) and osmolality >100mosmol/kg - in presence of hyponatraemia ( plasma Na+ <125mmol/K) - low plasma osmolality (<260mosmol/kg)
102
explain the pathology of SIADH
- excessive secretion or action of ADH - causes excessive water resorption - causing low Na in relation to water
103
what are the causes of SIADH
- maligancy - CNS disorders e.g SAH, stroke - chest disease e.g TB, pneumonia - endocrine - hypothyroidism - drugs: opiates, SSRI's
104
what is the treatment of SIADH
- treat cause and restrict fluid | - salt +/- loop diuretic
105
what is diabetes mellitus
- lack or reduced effectiveness of endogenous insulin causing hyperglycaemia - cases serious vascular problems: stroke, MI, renovascular disease, limb ischaemia
106
describe type 1 diabetes
- usually adolescent onset - caused by insulin deficiency from autoimmune destruction of insulin secreting pancreatic Beta cells - >90% HLA DR3+/-DR4 - concordance only 30% in identical twins- indicating environmental influence
107
describe type 2 diabetes
- caused by decreased insulin secretion and increased insulin resistance associated with obesity, lack of exercise, calorie and alcohol excess - increased prevalence in men, asians and the elderly - >80% concordance in identical twins, indicating stronger genetic influence than type 1 - typically progresses from impaired glucose tolerance (IGT) or impaired fasting glucose (IFG) - not HLA associated - asymptomatic/complications
108
what are the causes of diabetes
- steroids - anti HIV - pancreatitis, trauma, cancer, surgery, pancreatic destruction - cushings disease, acromegaly, hyperthyroid, pregnancy
109
what are the diagnostic criteria for diabetes (WHO)
-symptoms of hyperglycaemia ( polyuria, polydipsia, unexplained weight loss, visual blurring, genital thrush, lethargy) PLUS - a random venous plasma glucose concentration > or equal to 11.1mmol/l OR - a fastting plasma glucose concentation > or equal to 7mmol/L OR - two hour plasma glucose concentration > 11.1mmol/l two hours after 75 anhydrous glucose in an oral glucose tolerance test
110
what are the complications of diabetes
- hyperosmolar hyperglycaemic state (HHS) - type 2 - diabetic ketoacidosis- mainly type 1 - vascular disease - nephropathy - diabetic retinopathy - cataracts - neuropathy - ischaemia of feet - foot ulceration
111
descrobe the pathology, features and treatment of hyperosmolar hyperglycaemic state (HHS)
- high blood sugar results in increased osmolarity without significant ketoacidosis - dehydration, altered consciousness, weakness, leg cramps, trouble seeing - develops over days to weeks - low/normal ketones - treat with IV fluids, K+ replacement, insulin (make sure K+ high as insulin also causes movement of K+ into cells) LMWH prophylaxis
112
what is the pathology of diabetic ketoacidosis (DKA)
- excessive glucose but lack of insulin causes glucose to not be taken up into cells to be metabolised - body goes into starvation like state - gradual drowsiness, vomiting and dehydration - ketotic breath - triggered by infection, surgery, MI, pancreatitis, chemo
113
how is ketoacidosis diagnosed
- acidaemia ( venous blood PH < 7.3 or HCO3- <15mmol/L) - hyperglycaemia or known DM - ketonaemia or significant ketonuria ``` tests - ECG -CXR dipstick +MSU - blood- capillary and lab glucose, ketones, PH, bicarb, culture ```
114
what is the management of ketoacidosis
- replace volume then correct metabolic defects
115
describe neuropathy in DM
- decreased sensation in stocking distribution - absent ankle jerks - charcot joint - loss of pain sensation causes increased mechanical stress + repeated joint injury
116
what is the treatment of ischaemia of feet in DM
- doppler test ABPI - education - regular chiropody to remove callus - surgery e.g stents
117
what is the general management of DM
- education and lifestyle advice - exercise to increase insulin sensitivity - healthy eating (decreased saturated fats, decreased sugar, increased starch) - assess global vascular risk - start high intensity statin e.g atrovastatin - foot care - control BP
118
what is the specific management of type 1 DM
- insulin injections 1. ultrafast at start of meal or just after 2. isophane insulin (varibale peak at 4-12 hrs) 3. premixed 4. long acting recombinant human insulin analogues at bed time in type 1 or 2
119
what is the treatment for type 2 diabetes
1. lifestyle - diet, weight, exercise 2. monotherapy - 1st line = metformin - a biguanide which increases insulin sensitivity and decreases weight 3. if HbA1c rises to 58mmol/mol consider dual therapy with: - metformin + DPP4 inhibitor - metformin and proglitazone - metformin and sulphonylurea (SU) - metformin and SGLT- 2i 4. triple therapy 5. insulin or GLP analogues
120
what do DPP4 inhibitors do
- block DPP4 an enzyme which destroys hormone incretin - incretin stimulates insulin secretion when glucose in intestines usually e. g sitagliptin
121
what does proglitazone do
- increases insulin sensitivity
122
what does sulphonylurea do
- increases insulin secretion by opening channels in B cell | e. g gliclazide
123
what does SGLTi2 do
- selective sodium-glucose cotransporter 2 inhibitor - blocks resorption of glucose in kidneys and promotes excretion of excess glucose in urine e. g canafligozin
124
when is PTH usually secreted and what does it do
- in response to low calcium levels - increases osteoclast activity releasing cA2+ FROM BONES - increases Ca2+, decreases phosphate resorption from kidney - active 1,25 dihydroxyvitamin D3 production increase
125
what are the causes of hyperparathyroid
- adenoma - hyperplasia (primary) - renal failure (secondary)
126
what is the presentation of hyperparathyroid
1. of hypercalcaemia 2. of bone resorption - fractures, osteopenia/porosis 3. hypertension
127
what are the causes of hypoparathyroid
- gland failure (AI, congenital) (primary) | - radiation, surgery (secondary)
128
what are the symptoms of hypoparathyroid
- of hypocalcaemia +/- AI comorbidities - spasms -– Trousseau’s on inflation of cuff -anxious -seizures -Chvostek’s – tap facial nerve over parotid – corner of mouth twitches
129
what are carcinoid tumours
- tumours of enterochromaffin cell (neural crest) that are capable of producing 5HT (serotonin) - may secrete bradykinin, tachykinin, substance P, gastrin, insulin, glucagon, ACTH (cushings), parathyroid and thyroid hormones
130
what are the symptoms of carcinoid syndrome (hepatic involvement of tumour)
- bronchoconstriction - flushing - diarrhoea - CCF
131
how are symptoms of carcinoid tumour treat
- octreotide (somatostain analogue)
132
what are the risk factors for breast cancer
- family history - age - uninterrupted oestrogen exposure - 1st pregnancy >30 years - early menarche, late menopause - HRT - obesity
133
describe the link between BRCA genes and breast cancer
- 5-10 % of cancers due to mutation in BRCA1 or BRCA2 - both genes function as tumour suppressors - a cancer phenotype can be seen when one copy of the gene is normal - BRCA1 confers a 55-65% lifetime risk BRCA2 45% risk
134
when should you refer someone for genetic testing from breast cancer
- 1st degree relatives with breast cancer <40, male breast cancer, bilateral breast cancer <50 - 1st and 2nd degree with breast or ovarian - three 1st or 2nd degree relatives with breast cancer - risk assessment calculation of >3% in 10 years
135
what should you look for on a breast cancer examination/history
- previous lumps? - family history? nipple discharge? -skin changes? - pain? - change in size related to menstruation? - number of pregancies - first/last period - post natal? - drugs? - dimpling -nipple inversion - size shape of lump - fixed/tethered to skin or underlying structure - hard? - defined border?
136
when should you 2 week wait someone for breast cancer
- aged 30 and over with an unexplained breast lump - aged 50 and over with unilateral nipple changes of concern including discharge or retraction consider if - age 30 and over with unexplained axilla lump - skin changes suggestive of breast cancer
137
what are the three parts of the triple assessment for breast cancer
1. clinical exam 2. radiology, US for <35 years, mammogram + US for >35 years 3. histology/cytology (biopsy)
138
describe the breast cancer screening programme
- women aged 50-70 - mammograms - breasts xrayed - two xrays of each breast at different angles - about 1/25 called back for further assessment and about 1/4 of those have breast cancer
139
what is the staging of breast cancer
1. confined to breast, mobile 2. growth confined to breast, lymph nodes in ipsilateral axilla 3. tumour fixed to muscle 4. fixation to chest wall, metastases
140
what is the treatment of breast cancer
surgery - removal via wide local excision/masectomy +/- breast reconstruction radiotherapy - after removal (WLE) WIDE LOCAL EXCISION chemo - adjuvant chemo improves survival and reduces recurrance (after removal) endocrine agents e.g aromatase inhibitors target oestrogen and decrease synthesis
141
what is amyloidosis
- a group of disorders characterised by extracellular deposits of protein in fibrillar form resistant to degradation
142
what is the pathology of primary amyloidosis
- proliferation of plasma cell clone - amyloidogenic monoclonal immunoglobulins degradation fibrillar light chain protein deposition - organ failure associated with myeloma and lymphoma
143
what is the pathology of secondary amyloidosis
- amyloid is derived from serum amyloid A, an acute phase protein reflecting chronic inflammation in RA, UC/crohns, and chronic infections - TB, osteomyelitis, bronchiectasis
144
what is the definition of IGT
- fasting plasma glucose <7mmol/L and oral glucose tolerance (OGTT) 2h glucose >or equal to 7.8mmol/l but <11.1mmol/L
145
what is the definition of IFG
- fasting glucose > or equal to 6.1mmol/l bt <7mmol/L
146
describe diabetic nephropathy and its treatment
- due to hyperglycaemia causing increased growth factors, RAAS activation, oxidative stress to kidney which causes increased glomerular capillary pressure, endothelial and podocyte damage - microalbuminuria is the first sign = A:CR 3-30mg/mmol - control diabetes, BP <130/80, decrease sodium intake to 2g per day, statins to reduce CV risk
147
describe the types of retinopathy in DM
- background - microaneurysms (clots), haemorrhages (blots) and hard exudates (lipid deposits) - proliferative - new vessel form - maculopathy --- capillary endothelial change - vascular leak - microaneurysms - capillary occlusions -- local hypoxia + ischaemia -- new vessel formation
148
list the 5 main types of thyroid cancer
- papillary - follicular - medullary - lymphoma - anaplastic
149
which thyroid cancer most commonly effects younger patients and what is its treatment
- papillary - most common - spreads to lymph nodes and lung - total thyroidectomy +/- node excision +/- radioiodine - levothyroxine to suppress TSH
150
which thyroid cancer effects middle aged patients and what is its treatment
- follicular - spreads via blood to bone and lung - total thyroidectomy and T4 suppression and radioiodine
151
give three antibodies you would find in Graves disease
- Thyroid-stimulating immunoglobulin - antithyroglobulin antibodies - anti-thyroid peroxidase antibodies
152
what are the symptoms associated with graves disease
- thyroid associated opthalmology: swelling in extraocular muscles eye discomfort, grittiness, increased lacrimation, photophobia, diplopia, protrusion -acropatchy - clubbing and soft tissue swelling of the hands
153
what is onycholysis and what is it associated with
- painless seperation of the nail from the nail bed due to psoriasis
154
what is secondary hyperparathyroidism and what are the levels of serum Calcium and PTH
- secondary hyperparathyroidism is due to increased secretion of PTH in response to low serum calcium e. g by renal failure, vit d deficiency - high PTH - low calcium
155
what is primary hyperparathyroidism and what are the levels of serum Calcium and PTH
- high PTH - high calcium due to parathyroid adenoma or hyperplasia
156
what can be found on imaging for hyperparathyroid
pepperpot skull
157
what is the treatment of hyperparathyroid
- Mild – increase fluid – stones, avoid thiazides + high Ca2+ & vit D intake. Review 6 monthly. - Excision of adenoma/hyperplastic glands – usually if <50. Laryngeal nerve, hypoparathy. - Cinacalcet – increases sensitivity of parathyroid cells to Ca2+ - negative feedback – decreases PTH – monitor.
158
what are the tests for DI
-Dx – water deprivation test. Not drinking any water for several hours - if you have DI you will still pass lots of dilute urine Other Ix – U&E, Ca2+, glucose, serum and urine osmolalities.
Phase2a
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