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Phase2a > endocrine, derm + misc > Flashcards

endocrine, derm + misc Flashcards

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
Q

what is the pathology of acromegaly

A
  • 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
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26
Q

what are the symptoms and signs of acromegaly

A
  • 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
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27
Q

what are the complications of acromegaly

A
  • impaired glucose tolerance and DM
  • hypertension and heart disease
  • cerebrovascular events and headaches
  • arthritis
  • sleep apnea
  • neoplasia
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28
Q

criteria for diagnosis of acromegaly (exclusion)

A 
- 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
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29
Q

why are levels of GH unreliable in diagnosis of acromegaly

A
  • random GH secretion is pulsatile and during peaks acromegalic and normal levels overlap
  • GH increases also in stress, sleep, puberty and pregnancy
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30
Q

what tests can be used to diagnose acromegaly

A
  • Glucose tolerance test
  • Random GH (unreliable)
  • MRI of pituitary fossa
  • ECH, ECHO
  • old photos
  • visual field tests
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31
Q

what is the treatment of acromegaly

A
  • 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
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32
Q

what is a prolactinoma

A
  • lactotroph cell tumour of pituitary
  • 90 per 100000
  • women >men
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33
Q

what are the features of prolactinoma

A

local tumour effect

  • headache
  • visual field defect
  • CSF leak
  • menstrual irregularity
  • infertility
  • galactorrhoea - milky nipple
  • low libido
  • low testosterone in men
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34
Q

how is prolactinoma managed

A
  • dopamine agonists
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35
Q

what are the ways that a pituitary tumour can cause pathology

A
  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)
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36
Q

give examples of non functioning pituitary tumours

A
  • craniopharyngioma
  • meningioma
  • non functioning pituitary adenoma
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37
Q

describe the pathology and symptoms of craniopharyngioma

A
  • 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
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38
Q

which hypothalamic hormone causes release of thyroid stimulating hormone (TSH) from the anterior pituitary

A

thyrotropin releasing hormone (TRH)

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39
Q

Gonadotrophic releasing hormone (GnRH) causes release of which hormones from the anterior pituitary

A
  • follicular stimulating hormone (FSH)

- luteinizing hormone (LH)

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40
Q

dopamine (DA) released from the hypothalamus has what effect on the anterior pituitary

A

inhibits prolactin release

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41
Q

somatostatin released from hypothalamus causes what effect on anterior pituitary

A

inhibits release of GH

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42
Q

which hormone released from hypothalamus causes release of adrenocorticotrophic hormone (ACTH) from anterior pituitary

A
  • corticotrophin releasing hormone (CRH)
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43
Q

what is ACTH’s target organ and what does it cause

A
  • adrenal cortex - releases cortisol
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44
Q

what is produced in the adrenal cortex/where

A
  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
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45
Q

what is cushings syndrome

A

the clinical state induced by chronic glucocorticoid excess and loss of normal feedback mechanisms of the hypothalamopituitary adrenal axis

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46
Q

what are the causes of cushings syndrome

A
  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

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47
Q

what are the symptoms of cushings syndrome

A
  • 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
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48
Q

what are the tests for cushing’s syndrome

A
  • 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
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49
Q

what is the treatment of cushings syndrome

A
  • 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
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50
Q

what is addisons disease

A
  • primary adrenal insufficiency

- destruction of adrenal cortex leads to glucocorticoid and mineralcorticoid deficiency

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51
Q

what is the cause of Addisons disease

A
  • 80% autoimmune in UK
  • TB most common cause worldwide
  • adrenal metastases from lung, breast, renal
  • lymphoma
  • opportunistic in HIV
  • adrenal haemorrhage
  • congenital
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52
Q

what is the cause of secondary adrenal insufficiency

A
  • hypopituitarism (lack of ACTH) - due to:
  • pituitary macroadenoma/craniopharyngioma
  • hypophysitis (pituitary inflammation
  • mets
  • infection
  • RT
  • congenital
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53
Q

what is the cause of tertiary adrenal insufficiency

A
  • steroids suppressing pituitary axis
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54
Q

what are the symptoms of adrenal insufficiency

A
  • fatigue
  • weightloss
  • adrenal crisis
  • headache
  • poor recovery from illness
    -vomiting and abdo pain
    signs
  • pigmentation and pallor
  • hypotension
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55
Q

what are the tests for adrenal insufficency

A
  • 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
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56
Q

what is the treatment of adrenal insufficiency

A
  • hydrocortisone (pharmaceutical name for cortisol) 2-3x per day
  • aldosterone replacement w/ fludrocortisone (in primary)
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57
Q

what are the signs of adrenal crisis

A
  • Decreased Na+
  • increased K+
  • decreased glucose
  • fever
  • fatigue
  • hypotension and CV collapse
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58
Q

what is the management of adrenal crisis

A
  • 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
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59
Q

what is Conns syndrome

A
  • excess production of aldosterone causing inc Na and water retention, and decreased renin release due to solitary aldosterone producing adenoma
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60
Q

what are the symptoms of hyperaldosteronism

A
  • asymptomatic or of hypokalaemia: weakness, cramps, paraesthesiae, polyuria, hypertension
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61
Q

what are the causes of hyperaldosteronism

A

2/3 conn’s syndrome

1/3 due to bilateral adrenocortical hyperplasia

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62
Q

what are the tests for hyperaldosteronism

A
  • U+E
  • renin and aldosterone
  • dont rely on hypokalaemia
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63
Q

what is the treatment of hyperaldosteronism

A
  • Conn’s - laproscopic adrenalectomy and spironolactone 4 weeks pre op
  • hyperplasia - spironolactone or amiloride
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64
Q

give an example of secondary hyperaldosteronism

A
  • due to high renin from decreased renal perfusiong e.g renal artery stenosis, diuretics, hepatic failure
65
Q

what are the symptoms and signs of thyrotoxicosis/hyperthyroidism

A
  • 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
Q

what are the three mechanisms for thyrotoxicosis (increased thyroid hormones in blood)

A

a. overproduction of thyroid hormone (hyperthyroidism)
b. leakage of preformed hormone from thyroid
c. ingestion of excess thyroid hormone

67
Q

what are the tests for thyrotoxicosis

A
  • decreased TSH, increased T4 or T3
  • mild normocytic anaemia
  • mild neutropenia
  • inc ESR, inc LFT, inc Ca2+
  • check thyroid autoantibodies
68
Q

what are the causes of thyrotoxicosis

A
  • graves disease
  • toxic multinodular goitre
  • toxic adenoma
69
Q

what is graves disease/ pathology

A
  • 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
Q

what is toxic multinodular goitre

A
  • seen in elderly and iodine deficient areas

- nodules secrete thyroid hormones

71
Q

what is toxic adenoma

A
  • solitary nodule producing t3+t4

- hot nodule on isotope scan and rest of gland suppressed

72
Q

what is the treatment of thyrotoxicosis

A
  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
Q

what are the symptoms and signs of hypothyroidism

A
  • 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
Q

How is hypothyroid diagnosed

A
  • inc TSH

- decreased T4

75
Q

what are the causes of hypothyroidism

A

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
Q

what is the treatment of hypothyroidism

A
  • 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
Q

what are the signs and symptoms of hyperkalaemia

A
  • fast irregular pulse
  • chest pain
  • weakness
  • palpitations
78
Q

what will be found on an ECG for hyperkalaemia

A
  • tall tented T waves
  • small P
  • wide QRS
79
Q

what are the causes of hyperkalaemia

A
  • oliguric renal failure
  • K+ sparing diuretics
  • Addisons disease
  • metabolic acidosis (DM)
  • drugs e.g ACE-I
80
Q

what is the treatment for hyperkalaemia

A

non urgent - polystyrene sulfonate resin - binds K+ in gut preventing absorption
urgent - calcium chloride + insulin (which stimulates intracellular K+ uptake)

81
Q

what are the symptoms of hypokalaemia

A
  • muscle weakness
  • hypotonia
  • hyporeflexia
  • cramps
  • tetany
  • constipation
  • palpitations
82
Q

what is seen on an ECG when a pt has hypokalaemia

A
  • small or inverted t waves
  • prominent U waves
  • long PR interval
  • depressed ST
83
Q

what are the causes of hypokalaemia

A
  • diuretics
  • vomiting and diarrhoea
  • cushings syndrome/steroids/ACTH
  • Conn’s syndrome
  • alkalosis
  • pyloric stenosis
84
Q

what is the treatment of hypokalaemia

A
  • K+ supplements
85
Q

what are the signs and symptoms of hypercalcaemia

A
  • abdo pain
  • vomiting
  • constipation
  • renal stones
  • CA
  • hypertension
  • tiredness
  • confusion
86
Q

what is seen on an ECG when a pt has hypercalcaemia

A
  • decreased QT interval
87
Q

what are the causes of hypercalcaemia

A
  • maligancy
  • primary hyperparathyroidism
  • vit d intoxication
  • thyrotoxicosis
88
Q

what is the treatment of hypercalcaemia

A

bisphosphonates e.g alendronate

89
Q

what are the symptoms of hypocalcaemia

A
  • cramps

- paraesthesia

90
Q

what is seen on an ECG when a pt has hypocalcaemia

A
  • INCREASED QT
91
Q

what are the causes of hypocalcaemia

A
  • Vit D deficiency
  • osteomalacia
  • kidney disease
  • hypoparathyroidism
92
Q

what is the treatment of hypocalcemia

A

calcium supplementation

- calcium gluconate

93
Q

what are the symptoms + treatment of hypernatraemia

A
  • lethargy
  • thirst
  • weakness
  • confusion

treatment
H20!

94
Q

what are the causes of hypernatraemia

A
  • fluid loss without replacement

- diabetes insipidus

95
Q

what is diabetes insipidus/pathology

A
  • 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
Q

what are the symptoms of DI

A
  • polyuria (large volumes of urine)
  • of hypernatraemia
  • dehydration
  • polydipsia
97
Q

what are the causes of DI

A

nephrogenic

  • inherited
  • drugs
  • CKD
  • metabolic (decreased K+, increased Ca2+)

cranial

  • idiopathic
  • congenital
  • tumour e.g craniopharyngioma
  • AI hypophysitis
  • haemorrhage
  • hypophysectomy
98
Q

what is the treatment of DI

A

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
Q

what are the signs and symptoms of hyponatraemia

A
  • anorexia
  • nausea
  • malaise
  • headache
  • irritibility
  • confusion
  • weakness
100
Q

what are the causes of hyponatraemia

A

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
Q

how is syndrome of innappropriate ADH secretion diagnosed

A
  • concentrated urine (Na+ > 20mmol/L) and osmolality >100mosmol/kg
  • in presence of hyponatraemia ( plasma Na+ <125mmol/K)
  • low plasma osmolality (<260mosmol/kg)
102
Q

explain the pathology of SIADH

A
  • excessive secretion or action of ADH
  • causes excessive water resorption
  • causing low Na in relation to water
103
Q

what are the causes of SIADH

A
  • maligancy
  • CNS disorders e.g SAH, stroke
  • chest disease e.g TB, pneumonia
  • endocrine - hypothyroidism
  • drugs: opiates, SSRI’s
104
Q

what is the treatment of SIADH

A
  • treat cause and restrict fluid

- salt +/- loop diuretic

105
Q

what is diabetes mellitus

A
  • lack or reduced effectiveness of endogenous insulin causing hyperglycaemia
  • cases serious vascular problems: stroke, MI, renovascular disease, limb ischaemia
106
Q

describe type 1 diabetes

A
  • 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
Q

describe type 2 diabetes

A
  • 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
Q

what are the causes of diabetes

A
  • steroids
  • anti HIV
  • pancreatitis, trauma, cancer, surgery, pancreatic destruction
  • cushings disease, acromegaly, hyperthyroid, pregnancy
109
Q

what are the diagnostic criteria for diabetes (WHO)

A

-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
Q

what are the complications of diabetes

A
  • hyperosmolar hyperglycaemic state (HHS) - type 2
  • diabetic ketoacidosis- mainly type 1
  • vascular disease
  • nephropathy
  • diabetic retinopathy
  • cataracts
  • neuropathy
  • ischaemia of feet
  • foot ulceration
111
Q

descrobe the pathology, features and treatment of hyperosmolar hyperglycaemic state (HHS)

A
  • 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
Q

what is the pathology of diabetic ketoacidosis (DKA)

A
  • 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
Q

how is ketoacidosis diagnosed

A
  • 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
Q

what is the management of ketoacidosis

A
  • replace volume then correct metabolic defects
115
Q

describe neuropathy in DM

A
  • decreased sensation in stocking distribution
  • absent ankle jerks
  • charcot joint
  • loss of pain sensation causes increased mechanical stress + repeated joint injury
116
Q

what is the treatment of ischaemia of feet in DM

A
  • doppler test ABPI
  • education
  • regular chiropody to remove callus
  • surgery e.g stents
117
Q

what is the general management of DM

A
  • 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
Q

what is the specific management of type 1 DM

A
  • 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
Q

what is the treatment for type 2 diabetes

A
  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
Q

what do DPP4 inhibitors do

A
  • block DPP4 an enzyme which destroys hormone incretin
  • incretin stimulates insulin secretion when glucose in intestines usually
    e. g sitagliptin
121
Q

what does proglitazone do

A
  • increases insulin sensitivity
122
Q

what does sulphonylurea do

A
  • increases insulin secretion by opening channels in B cell

e. g gliclazide

123
Q

what does SGLTi2 do

A
  • selective sodium-glucose cotransporter 2 inhibitor
  • blocks resorption of glucose in kidneys and promotes excretion of excess glucose in urine
    e. g canafligozin
124
Q

when is PTH usually secreted and what does it do

A
  • 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
Q

what are the causes of hyperparathyroid

A
  • adenoma
  • hyperplasia
    (primary)
  • renal failure
    (secondary)
126
Q

what is the presentation of hyperparathyroid

A
  1. of hypercalcaemia
  2. of bone resorption - fractures, osteopenia/porosis
  3. hypertension
127
Q

what are the causes of hypoparathyroid

A
  • gland failure (AI, congenital) (primary)

- radiation, surgery (secondary)

128
Q

what are the symptoms of hypoparathyroid

A
  • 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
Q

what are carcinoid tumours

A
  • 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
Q

what are the symptoms of carcinoid syndrome (hepatic involvement of tumour)

A
  • bronchoconstriction
  • flushing
  • diarrhoea
  • CCF
131
Q

how are symptoms of carcinoid tumour treat

A
  • octreotide (somatostain analogue)
132
Q

what are the risk factors for breast cancer

A
  • family history
  • age
  • uninterrupted oestrogen exposure
  • 1st pregnancy >30 years
  • early menarche, late menopause
  • HRT
  • obesity
133
Q

describe the link between BRCA genes and breast cancer

A
  • 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
Q

when should you refer someone for genetic testing from breast cancer

A
  • 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
Q

what should you look for on a breast cancer examination/history

A
  • 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
Q

when should you 2 week wait someone for breast cancer

A
  • 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
Q

what are the three parts of the triple assessment for breast cancer

A
  1. clinical exam
  2. radiology, US for <35 years, mammogram + US for >35 years
  3. histology/cytology (biopsy)
138
Q

describe the breast cancer screening programme

A
  • 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
Q

what is the staging of breast cancer

A
  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
Q

what is the treatment of breast cancer

A

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
Q

what is amyloidosis

A
  • a group of disorders characterised by extracellular deposits of protein in fibrillar form resistant to degradation
142
Q

what is the pathology of primary amyloidosis

A
  • proliferation of plasma cell clone
  • amyloidogenic monoclonal immunoglobulins degradation fibrillar light chain protein deposition
  • organ failure

associated with myeloma and lymphoma

143
Q

what is the pathology of secondary amyloidosis

A
  • 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
Q

what is the definition of IGT

A
  • fasting plasma glucose <7mmol/L and oral glucose tolerance (OGTT) 2h glucose >or equal to 7.8mmol/l but <11.1mmol/L
145
Q

what is the definition of IFG

A
  • fasting glucose > or equal to 6.1mmol/l bt <7mmol/L
146
Q

describe diabetic nephropathy and its treatment

A
  • 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
Q

describe the types of retinopathy in DM

A
  • 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
Q

list the 5 main types of thyroid cancer

A
  • papillary
  • follicular
  • medullary
  • lymphoma
  • anaplastic
149
Q

which thyroid cancer most commonly effects younger patients and what is its treatment

A
  • papillary - most common
  • spreads to lymph nodes and lung
  • total thyroidectomy +/- node excision +/- radioiodine
  • levothyroxine to suppress TSH
150
Q

which thyroid cancer effects middle aged patients and what is its treatment

A
  • follicular
  • spreads via blood to bone and lung
  • total thyroidectomy and T4 suppression and radioiodine
151
Q

give three antibodies you would find in Graves disease

A
  • Thyroid-stimulating immunoglobulin
  • antithyroglobulin antibodies
  • anti-thyroid peroxidase antibodies
152
Q

what are the symptoms associated with graves disease

A
  • 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
Q

what is onycholysis and what is it associated with

A
  • painless seperation of the nail from the nail bed due to psoriasis
154
Q

what is secondary hyperparathyroidism and what are the levels of serum Calcium and PTH

A
  • 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
Q

what is primary hyperparathyroidism and what are the levels of serum Calcium and PTH

A
  • high PTH
  • high calcium
    due to parathyroid adenoma or hyperplasia
156
Q

what can be found on imaging for hyperparathyroid

A

pepperpot skull

157
Q

what is the treatment of hyperparathyroid

A
  • 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
Q

what are the tests for DI

A

-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 (10 decks)

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