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Chem Path Flashcards

1
Q

How is calcium divided up around the body

A

99% skeleton

1% serum

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2
Q

Forms of serum calcium

A

Free ‘ionised’ - 50%
Protein bound - 40% - to albumin
Complexed - 10% - citrate/phosphate

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3
Q

Calculating total calcium from ionised Ca.

Corrected calcium equation

Normal serum calcium

A 
Double ionised (If albumin is constant)
Total iron is what's given on lab tests so can use corrected ca formula to see if there is true increase/decrease in free ionised iron or if albumin is affecting

Serum calcium + 0.02(40-serum albumin)

2.2-2.6mmol/L

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4
Q

Which form of calcium in serum matters and why

A

Free ionised

Ca important in muscle depolarisation and nerve + muscle control

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5
Q

Effect of high albumin on free calcium

A

low (more bound)

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6
Q

Effect of low albumin on free calcium

A

high (less bound)

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7
Q

Hormones involved in calcium homeostasis

A 
PTH
Vit D (steroid hormone) - cholecalciferol (D3) is animal form
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8
Q

Summary of PTH function

A

Calcium absorption via 3 sources
Bone
Kidney (reabsorbs + Stimulates 1,25 (OH)2 vit D synthesis (1 alpha hydroxylation))
Gut (by vit D)

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9
Q

Process of Vit D synthesis

A

D3 synthesised in skin

Liver:
25-hydroxylation
(stored and measured form of vit D) - is inactive

Kidney - where activated
1 alpha hydroxylation (under PTH)

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10
Q

Roles of calcitriol

1,25 - dihydroxycholecalciferol

A

Intestinal Calcium absorption
Intestinal phosphate absorption
Bone formation

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11
Q

Roles of the skeleton (metabolic)

A

Metabolic role in calcium homeostasis

Main reservoir of calcium, phosphate and magnesium

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12
Q

Roles of the skeleton (orthopaedic)

A 
Structural framework
Strong
Lightweight
Mobile
Protect organs
Capable or orderly growth and remodelling
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13
Q

Metabolic bone disorders

A

1) Osteoporosis
2) Osteomalacia
3) Paget’s disease

Parathyroid bone disease
Renal osteodystrophy

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14
Q

Vit D deficiency clinical picture children

A 
Defective bone mineralisation - Rickets
Frontal bossing
Bowed legs (tibia)
Widened epiphyses ar wrists
Myopathy
Costochondral swellings
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15
Q

Vit D deficiency clinical picture adults

A 
Osteomalacia - demineralised bone
Bone and muscle pain
Increased fracture risk
Low Ca + Pi, raised ALP
Looser's zones
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16
Q

Osteomalacia in adults causes

A

Vit D deficiency:

  • Renal failure (1alpha hydroxylase lack)
  • Anticonvulsants (break down vit D)
  • Lack of sunlight
  • Chapatis (phytic acid) - questionable
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17
Q

What is osteoporosis

A

Normal bone but less - normal aging, normal biochem

Loss of bone density. Asymptomatic until first fracture

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18
Q

How is osteoporosis diagnosed

Score used
and meaning

A

DEXA scan - hip( femoral neck) + lumbar spine

T score >2.5 SD below normal

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19
Q

T score use
vs
Z score use

A

T score: sd from mean of healthy young pop
fracture risk

Z score: sd from mean of age-matched controls
accelerated bone loses in younger pts

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20
Q

Osteoporosis causes

A

Age, post menopausal: Primary reasons
Drugs (steroids), systemic diseases: Secondary reasons

Risk factors: Sedentary, Smoker, Shotter slim, childhood illness. Cushings, thyrotoxicosis, early menopause, hyperprolactinaemia,
Genetics, prolonged illness

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21
Q

Osteoporosis tx

A

Weight bearing ex
Stop smoking
Reduce alcohol

Drugs: Vit D/Ca
Bisphosponates (alendronate) - decrease bone resorption
Teriparatide
Strontium
Oestrogens - HRT
SERM - e.g. raloxifene
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22
Q

Bisphosphonates side effecct

A

GI

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23
Q

Hypocalcaemia signs

A

Neruomuscular excitability

  • Trousseau
  • Hyperreflexia
  • Chovstek’s sign
  • Convulsions
  • Prolonged Q-T
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24
Q

Aetiology of Hypocalcaemia dependent on

A

1) PTH driven - low PTH
- Surgery (thyroidectomy)
- Autoimmune hypoparathyroid
- DiGeorge syndrome
- Mg deficiency (needed for PTH production

2) Non-PTH driven
- Vit D deficiency
- CKD (1-alpha hydroxylation)
- PTH resistance (pseudohypoparathyroid)

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25
Q

Biochem in secondary hyperparathyroidm

A

High PTH, low CA (lowest ever)

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26
Q

Response of PTH to hypocalcaemia if not due to low PTH

A

Secondary hypoparathyroid

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27
Q

Hypercalcaemia clinical picture

A

Polyuria, polydipsia, constipated, neuro confusion (seizures, coma - unlikely unless ca>3)

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28
Q

Hypercalcaemia aetiology dependent on

A

1) PTH suppression
- Malignancy - humoral, bone mets, haem
- Sarcoid (non renal 1a hydroxylation)
- Vit D excess (sunbeds)
- Thyrotoxicosis (thyroxine resorbs bone)
- thiazide diuretics

2) PTH not suppressed = PTH regulatory problem
- primary hyperparathyroidism

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29
Q

Hypercalcaemia tx

A 
FLUIDS
FLUIDS
FLUIDS
Bisphosphontes (IF CANCER ELSE NO)
TX underlying cause
Fluids = 0.9% saline
Use frusemide (lose calcium in urine)
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30
Q

Causes of secondary hyperparathyroidism

A

Low ca –> High PTH

Low vit D/ malabsorption
CKD
Pseudohypoparathyroid

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31
Q

What is Paget’s disease

A

Focal bone remodelling - lytic and sclerotic lesions
Warn, deformity, fracture, malignancy. Conductive and sensorineural hearing loss

Disorder of bone turnover
Skull and vertebrae aka axial

1) Osteolytic
2) Osteolytic-osteosclerotic
3) Quiescent osteosclerotic,

Elevated ALP
RAPID bone turnover on Nuclear med scan/XR
Mosaic lines

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32
Q

Normal GFR

A

120ml/min

Above 90 is normal

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33
Q

Definition of renal clearance

Use

A

Volume of plasma completely cleared of a marker substance.. per unit time

Can be used to calculate GFR

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34
Q

Renal clearance formula

A

C=(UxV)/P

U= urinary conc of marker
V = volume (needs to be /min so work out)
P= plasma conc of marker
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35
Q

Conditions of a marker for renal clearance

A

1) Freely filtered by glomerulus
2) Not secreted/absorbed by tubular cells
3) Not bound to serum proteins

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36
Q

Gold standard marker for measuring GFR

Limitation

A

Inulin - freely filtered, neutral charge, not processed by tubular cells

Needs steady state infusion - research tool only

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37
Q

Endogenous markers of GFR

A

Urea - first

  • by product of protein metabolism
  • freely filtered by glomerulus
  • variable (30-60%) resorption by tubular cells
  • Highly dependent on nutrition, hepatic function and if GI bleed aka useless

Serum creatinine - derived from muscle cells

  • Actively secreted into urine by tubular cells
  • Cr generation varies according to muscle, age, sex, ethnicity
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38
Q

What is eGFR
Formula used to calculate

Problem

A

To estimate creatinine clearance

eGFR-EPI
Takes into account age, sex, serum creatinine and ethnicity

Still imprecise at higher GFRs

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39
Q

Alternative to serum creatinine for eGFR

A 
cystatin C
produced by all nucleated cells
Constantly generated
Freely filtered
Almost completely reabsorbed and catabolised by tubular cells
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40
Q

What is the use os single injection GFR measurement

A

Pre chemo

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41
Q

Value of serum creatinine measurement

A

To determine change in renal function within an individual over time
- trend more valuable than actual value.

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42
Q

What is measured on a urine dip

A 
pH: 4.5-8
Specific gravity: 1.003-1.035
Protein
Blood
Leucocyte esterase: -ve result is significant
Nitrite: detects bacteria, esp gram -ve
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43
Q

AKI with calcium oxalate crystals on urine microscopy

Dx

A

Ethylene glycol poisoning (aka anti-freeze)

  • was metabolised to glycolic acid
  • glycolic acid metabolised to oxalic acid
  • oxalic acid binds to calcium containing stones
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44
Q

Casts seen on urine microscopy indicated that the problem is where?

A

Glomerulus

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45
Q

Suspected renal stone - choice of imagine

A

CT-KUB

Can do US-KUB after to look for hydronephrosis

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46
Q

Types of renal imaging

A 
Plain KUB
IVU
CT
US: Can differentiate CKD (shrivelled) and AKI/ look or hydronephrosis/ do a nephrostomy if kidney obstructed
MRI
Functional imaging - useful in paeds
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47
Q

AKI vs CKD

A

AKI

  • Abrupt GFR decline in days
  • Potensh reversible
  • Tx of precise diagnosis and reversing disease

CKD

  • Longstanding decline in GFR
  • Irreversible
  • Tx to prevent complications and limit progression
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48
Q

AKI definition

A

Rapid reduction in kidney function, leading to an inability to maintain electrolyte, acid-base and fluid homeostasis

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49
Q

AKI stages

A

1: ↑ sCr by >26micromol/L OR 1.5-1.9x reference sCr
2: ↑sCr by 2.0-2.9 reference sCr
3: ↑sCr by >3 reference sCr, or increase by >354 micromol/L

> means >/=

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50
Q

Causes of pre-renal AKI

A 
True volume depletion - most common
Hypotension
Oedematous
Selective renal ischaemia (RAS)
Drugs affecting glomerular blood flow
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51
Q

Drugs that predispose to AKI

A

NSAIDs: Decrease afferent arteriole dilation
Cacineurin inhibitors: Decrease afferent arteriole dilation
ACEi/ARBs: Decrease efferent arteriole constriction
Diuretics: Affect tubular function, decrease preload

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52
Q

What is ATN

Management

A

Acute tubular necrosis
Death of tubular cells - does not respond to restoration of circulating volume unlike pre-renal AKI

Dialyse for 3 weeks, should recover

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53
Q

Intrisic renal AKI causes

A

Abnormality in ANY part of the nephron

  • Vascular disease: vasculitis
  • Glomerular: glomerulonephritis
  • Tubular: ATN
  • Interstitial: analgesic nephropathy
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54
Q

Mechanisms of direct tubular injury in AKI

A
  • Mostly pre-renal AKI causing ATN
  • Endogenous toxins: Myoglobin/immunoglobuline
  • Exogenous toxins: contrast, aminoglycosides, amphotericin, acyclovir
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55
Q

Presentation of rhabdomyolysis induced AKI

A

Muscle weaknes

Dark urine + kidney injury

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56
Q

Rash (non-blanching, purpuric) + AKI

A

Systemic vasculitis

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57
Q

Immune dysfunction causing renal inflammation causes

A

Vasculitis
Glomerulonephritis

Dx on biopsy

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58
Q

Infiltration/abnormal protein deposition in AKI causes

A

Amyloidosis
Lymphoma
Myeloma

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59
Q

Post-renal AKI causes

A

Physical obstruction to urine flow

  • Intra-renal
  • Ureteric obstruction (bilateral) - prostate/urethral
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60
Q

What is obstructive uropathy

Pathophysiology

A

Hydronephrosis
GFR depends on hydraulic pressure gradient.
Obstruction increases tubular pressure
Immediate decrease in GFR

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61
Q

Obstructive uropathy recovery

A

Immediate relief of obstruction restores GRR fully with no structural damage. But if prolonged, there is structural damage

  • Glomerular ischaemia
  • Tubular damage
  • Long term interstitial scarring
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62
Q

Measures for defining AKI severity

A 
sCr as surrogate of GFR
Urine output (needs full time nurse)
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63
Q

CKD stages

A

1: GFR >90 (norm)
2: GFR 60-89 mild
3: GFR 30 -59 mod
4: GFR 15-29 sev,,
5: GFR <15/dialysis ESRF

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64
Q

Worst outcomes in CKD

A

lowest GFR
and
higher albumin:Cr

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65
Q

Causes of CKD

A 
Diabetes
HTN
Atherosclerotic renal disease
Chronic glomerulonephritis
Obstructive/infective urpoathy
Polycystic kidney
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66
Q

Roles of the kidney

A 
Excretion of water-soluble waste
Water balance
Electrolyte homeostasis
Acid-base homeostasis
Endocrine: EPO, RAS, vit D
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67
Q

Consequences of CKD

A 
Hormonal function decline:
- Anaemia
- Renal bone disease
Homeostatic decline
- Acidosis
- Hyperkalaemia
CVD
- Vascular calcification
- Uraemic cariomyopathy
Uraemia and death
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68
Q

Renal acidosis in CKD

Tx

A

Metabolic acidosis - failing to excrete protons

  • -> Muscle and protein degradation
  • -> Osteopenia due to mobilization of bone Ca
  • -> Cardiac dysfunction

Tx: oral sodium bicarbonate when serum bicarb <20

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69
Q

Hyperkalaemia in CKD

A

Potassium is major intracellular ion. Hyperkalaemia causes membrane depolarization, which is important in:

  • Cardiac function
  • Muscle function
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70
Q

Hyperkalaemia ECG changes

A

Peaked T waves
Flattened P waves
Broader QRS

Can get tachy, VF, cardiac arrest

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71
Q

High potassium foods

A

Milk
Choc
Dried fruits
Tomatoes

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72
Q

Anaemia of chronic renal disease

A

Progressive decline in EPO producing cells (necrosis) + loss of renal parenchyma

Usually when GFR <30
Normochromic, normocytic anaemia

Distinguish from other causes of anaemia that are common

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73
Q

Treatment of anaemia of CKD

No response to tx: causes

A

ESA

1) Fe deficiency
2) TB
3) Malignancy
4) B12 and folate deficiency
5) Hyperparathyroidism

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74
Q

Real bone disease in CKD

A

Reduced bone density (osteopenia), bone pain and fractures

  • Osteitis fibrosa cystica
  • Osteomalacia
  • Adyndamic bone disease
  • Mixed osteodystrophy
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75
Q

Effect of CKD on PTH

A

CKD = phosphate retention –> increased FGF-23 (makes you pee it out)
CKD also = decrease calcitriol
–> hypocalcaemia&raquo_space; sensed by parathyroid –> secondary hyperparathyroid

Bone becomes more resistant to PTH
Decreased Ca sensor
Decreased calcitriol sensor

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76
Q

What is osteitis fibrosa

X-ray features

Histopath features

A

Occurs in HyperPTH (Can occur in CKD)
Osteoclast resorption of caclified bone + replaced by fibrous tissue

Trabeculae become larger - blackened bits on x-ray. Cystic??

Brown’s tumours - many multinucleate giant cells

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77
Q

What is adynamic bone disease

Tx

A

In CKD
Excess suppression of PTH –> low bone turnover and reduced osteoid formation

Can suppress PTH using vit D or phosphate binders

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78
Q

Tx of CKD bone diseases

A 
Phosphate control
- Diet + phosphate binders
Vit D receptor activators
- 1-alpha calidol (mainstay)
- paricalcitol
Dirtect PTH suppression
- Cinacalcet
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79
Q

CVD in CKD mechanism

A

Most important consequence of CKD

- Risk of CVE directly predicted by GFR

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80
Q

Uraemic cardiomyopathy mechanism in CKD

A

LV hypertrophy
LV dilation
LV dysfunction

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81
Q

Contraindications to renal transplant

A

Active sepsis

Malignant disease within last 2 years

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82
Q

Normal pH on blood gas

A

7.35-7.45

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83
Q

Normal H+ in ECF

A

35-45nmol/l

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84
Q

Proton (H+) metabolism

A

Metabolism of fats, carbs and proteins produces carbon dioxide, water and hydrogen ions
~50-100mmol H+ produced per day
Excreted by kidney

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85
Q

Buffering of hydrogen ions is by what

A

Bicarbonate (ECF, glomerular filtrate)
Hb (RBC)
Phosphate (Intracellular, Renal tubular fluid)

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86
Q

Metabolism of CO2

A

Metabolism of fat, carbs and proteins produces co2, water and hydrogen ions
CO2 20,000-25,000 mol/day produced
Excreted by lung

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87
Q

What is the main control of respiration

A

Chemoreceptors in the hypothalamic respiratory centre.

Any increase in CO2 stimulates respiration thus maintaining a stable conc. of CO2

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88
Q

Metabolic acidosis causes

A

Increased H+ production e.g. DKA
Decreased H+ excretion e.g. renal tubular acidosis; renal failure
Bicarbonate loss e.g. intestinal fistula

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89
Q

Uncompensated metabolic acidosis changes to ABG

Compensated metabolic acidosis changes to ABG

A

High H+
Low bicarbonate

High H+
Low bicarbonate
Low CO2
- can’t compensate if resp failure - H+ will rise more

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90
Q

Acute Respiratory acidosis changes on ABG

Chronic Respiratory acidosis changes on ABG

A

High CO2; high H+; high HCO3-

High CO2; normalised H+; high HCO3-
PH may be normal now

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91
Q

Respiratory acidosis causes

A

Poor ventilation
Poor perfusion
Impaired gas exchange

If chronic
COPD
Emphysema

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92
Q

Causes of metabolic alkalosis

A

Hypokalaemia
H+ loss e.g. pyloric stenosis, vomiting
Ingestion of bicarbonate (tx for GI ulcer)

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93
Q

Cause of respiratory alkalosis

A

Hyperventilation

  • Anxiety
  • Hypoglycaemia
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94
Q

Aspirin overdose effect on ABG

A

Mixed metabolic acidosis and respiratory alkalosis
Hyperventilation stimulated
Hydrogen excretion by kidney

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95
Q

Haematuria causes

A

Nephritis - painless haematuria
Subacute endocarditis - FUO and microscopic bacteriuria
Acute rheumatic fever - child with sore throat
Renal stones - pain

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96
Q

Biochem in primary hyperparathyroidism

A

High Ca, High/norm PTH, low Ph, high/norm ALP, norm Vit D

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97
Q

What are Looser’s zones

A

Wide, transverse lucencies traversing part way through a bone - pesudofractures
Associated with Vit D deficiency - osteomalacia

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98
Q

Primary hyperPTH symptoms

A

Moans - depression
Stones - renal
Groans - abdo pain, pancreatitis
Bones - fractures

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99
Q 
Radial cystic changes
Browns tumours (what is it)
Associated with what condition
A

Primary hyperPTH

Brown’s tumour = osteitis fibrosa cystica - many multinucleate giant cells

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100
Q

Hypercalcaemia symptoms

A

Moans, bones, groans, stones
Asymptomatic
Polyuria/polydipsia
Band keratopathy (if present for long time e.g. primary hyperPTH)
Complications: Osteitis fibrosa, pancreatitis, renal stones, peptic ulcer, skeletal changes

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101
Q

Which diuretic can you use in hypercalcaemia and which to avoid

A 
Use frusemide (lose calcium in urine)
Avoid thiazides (don't lose calcium in urine)
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102
Q

Hypercalcaemia tx

A

0.9% saline

frusemide in case of pulmonary oedema

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103
Q

What are purines

A

Ubiquitous biomolecules

Adenosine, guanosine, inosine

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104
Q

Roles of purines

A

Part of the genetic code (A and G)
Second messengers for hormone action e.g. cAMP
Energy transfer e.g. ATP

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105
Q

Purine catabolism

A

Purine –> Hypoxanathine –> xanathine –> urate –> Allantoin
Step 2+3 requires XO
Step 4 requires uricase (not in humans)

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106
Q

Challenges of excreting urate

A

Insoluble

Circulates at conc close to it’s limit of solubility

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107
Q

Why is urate so close to it’s limit of solubility in our body?

A

Tubular urate handing

  • reabsorbed, resecreted multiple times
  • ultimately only 10% secreted
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108
Q

Purine synthesis

A 
De novo (less efficient, only norm occurring in BM where other pathway is insufficient)
Salvage pathway: recycling - needs HGPRT (HPRT)
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109
Q

Rate limiting step of purine synthesis

Controls

A

Catalysed by PAT

  • Inhibition by ANP and GNP
  • Positive feedback by PPRP
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110
Q

IEM - Purine

A 
Lesch Nyhan syndrome
HGPRT deficiency 
Normal at birth 
6/12 developmental delay
Choreiform movements, spasticity, mental retardation
Self mutilation

No ANP and GNP to inhibit PAT
- de novo pathway goes into overdrive, more catabolism of inosinic acid –> urate levels build up in blood
PPRP also builds up which drives PAT

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111
Q

Thiazide diuretics may cause what on bloods

A

Hypocalcaemia
Hyponatraemia
Hypoglycaemia
Hyperuricaea

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112
Q

Gout crystals are

Diagnosis

A

monosodium urate

Tap effusion
Polarised light
Red filter

Negatively birefringent needles perpendicular to axis of compensation

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113
Q

Gout acute vs chronic

A 
Podagra
- acute arthropathy
 vs 
Tophaceous gout
- chronic build up
- periarticular
- ear lobes and hands
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114
Q

Acute gout tx

A

NSAIDs - reduce inflammation e.g. diclofenac but avoid in CKD, asthmatics, peptic ulcer disease
Colchicine - inhbits microtubule formation, inhibiting neutrophil motility, can’t get into joints and react to presence of urate crystals
Glucocorticosteroids - anti-inflammatory

DO NOT BRING DOWN URATE LEVELS ACUTELY

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115
Q

Non-acute gout tx

A

Water, stop alcohol, reduce dietary urate (sardines, liver)
Reverse causing factors e.g. diuretics
Allopurinol inhibits XO
Increase renal excretion of urate with a uricosuric e.g. probenecid

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116
Q

Allopurinol used for
MOA
Contraindications

A

non-acute gout
Inhibits XO - reduces urate production
Azathioprine (az metabolite is metabolised by XO - can render patients neutropenic)

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117
Q

NSAID cautions/CI

A

Toxic to kidneys - avoid in CKD

CI in asthmatics and peptic ulcer

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118
Q

Pseudogout crystals

Dx

A

Pyrophosphate
Knee and shoulder

Tap effusion
Polarised light
Red filter

Positively birefringent needles parallel to axis of compensation

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119
Q

Hyponatraemia cut off

A

<135mmol/L

120
Q

Pathogenesis of hyponatraemia

A

Almost always due to excess water (extracellular) with no change in Na so conc is lower

121
Q

Hormone controlling Na levels

A

ADH (vasopressin)

122
Q

ADH action

A

Acts on collecting ducts on V2 receptors
Insertion of aquaporin 2
Water reabsorption

If high conc, will also act on V1 receptors - vasopressor effects (smooth muscle)

123
Q

What stimulates ADH secretion

A

1) High serum osmolality detected by hypothalamic osmoreceptors
2) Low blood volume/pressure detected by baroreceptors in carotids, atria, aorta

124
Q

1st thing to do in a patient with hyponatraemia

A

Clinical assessment of volume
Urine sodium - low is most reliable sign of hyponatraemia

Hypovolaemia: Dry mucus membranes, decreased skin turgor, JVP not visible

Hypervolaemia: Peripheral oedema, raised JVP

Difficult to distinguish between hypovolaemic and euvolaemic patients

125
Q

Signs of hypovolaemia

A 
Tachycardia
Postural hyptension
Dry mucus membranes
Reduced skin turgor
Confusion/drowsy
Reduced UO
Low urine Na <20

DO URINE SODIUM (kidneys reabsorb water and salt when hypovolaemic)

126
Q

When in hyponatraemis is urine sodium not helpful

A

Pts on diuretics - have to stop diuretics before checking

127
Q

Causes of hyponatraemia in hypovolaemic changes

A

Extra renal: d+V –> fluid loss –> hypovolaemia –> barorecepters stimulate –> ADH increased –> water resorption –> hyponatraemia

Renal: Diuretics will cause hyponatraemia ONLY when recenly started

128
Q

Hypervolaemia clinical signs

A

Raised JVP
Bibasal crepls
Peripheral oedema

129
Q

Causes of hyponatraemia in hypervolaemic pts

A

Failure

1) HF: Reduce CO –> Low BP –> excess ADH –> too much water
2) Cirrhosis: Patients vasodilate (due to NO) –> lower BP –> increase ADH
3) Renal failure: not excreting water

130
Q

Causes of hyponatramia in euvolaemic patients

A

All Endo

1) Hypothyroid: Reduced cardiac contractilty, reduces CO –> low BP –> ADH
2) Adrenal insufficiency: May cause hypovolaemia or pt may be euvolaemic because they need water for cortisol excretion
3) SIADH

131
Q

SIADH causes

A 
Any CNS pathology
Any lung pathology
Tumours - any
Post-surgery
Drugs (SSRI, TCA, opiates, PPI, carbamazepine)
132
Q

SIADH effect on sodium and osmolality

A

Excess ADH - retain more water - detected by atria - ANP release –> natriuresis (lose sodium and excess water with that) - euvolemic

Low plasma osmolality (~275-295mmol/kg)
High urine osmolality (>100)

133
Q

SIADH electrolyte abnormality and fluid status

A

Low Na
Euvolaemic

More ADH - retain water
Atria detects BP - natriuresis (lose Na and excess water)

134
Q

SIADH dx

A

No hypovolaemia
No hypothyroidism
No adrenal insufficiency

Reduced plasma osmolality
Increased urine osmolality (>100)

135
Q

SIADH tx

A

Do NOT give saline - will decrease sodium more –> fits –> death
- Fluid restrict

Demecleocycline - reduces responsiveness of CDT cells to ADH
Tolvaptan: V2 receptor antagonist
Can also use a combination of salt and loop diuretic

136
Q

Treatment of hyponatraemia

A

If hypovolaemic

  • replace with 0.9% saline
  • Ensure NOT SIADH

If hypervolaemic

  • Fluid restrct
  • Tx underlying cause

If euvolaemic

  • Fluid restrict
  • Tx underlying cause
  • Exclude tumour - head and chest imaging, examine, inc breast
137
Q

Treatment of severe hyponantraemia

A

ONLY IF reduced GCS and fitting

  • Tx seizures
  • Expert help
  • Hypertonic saline (2.7%)
138
Q

Hypernatraemia cut off

A

> 145

139
Q

Hypernatraemia causes

A

Water loss not replaced

  • GI, sweat
  • Renal loss - osmotic diuresis (DM uncontrolled), reduced ADH release/action (DI)

Patient can’t control water intake e.g. child/elderly - safeguarding issue

140
Q

Diabetes insipidus symptoms

A

Polyuria

Polydipsia

141
Q

Investigating diabetes insipidus

A

Serum glucose: Exclude DM
Serum K: Exclude hypokalaemia
Serum Ca: Exclude hypocalcaemia

Altered Ca and K can cause nephrogenic DI (kidney resistant to ADH actions)

Plasma and urine osmolaltity
WATER DEPRIVATION TEST
normal: urine will concentrate
DI: Won't concentrate urine (<300)
(Nephrogenic will not concentrate even with desmopressin)
142
Q

Hypernatraemia tx

A

Fluid replace with water ideally (dextrose if acute)

If hypovalaemic

  • 0.9% to correct ECF depletion
  • Dextrose to correct water deficit

Serial Na measurements every 4-6hours
Tx underlying cause

143
Q

Hallmarks of inherited metabolic disorders

A

Lack of end product
Build up of precursors
Abnormal, toxic metabolites

144
Q

What is phenylkotenouria

A

Phenylalanine hydroxylase deficiency
- build up of phenylalanine in blood

IQ <50 (toxic to CNS)

145
Q

Which IEM associated with low IQ

Test
Tx

A

Phenylketonuria
IQ<50

Blood Phe
Effective tx if started early in 1st 6 weeks of life

146
Q

What is sensitivity

A

True positive/Total disease present

147
Q

What is specificity

A

True negative/Total disease absent

148
Q

PPV

A

Positive predictive value

True positive/Total positive

149
Q

NPV

A

Negative predictive value

True negative/total negative

150
Q

PPV for PKU

A

80%

151
Q

Congenital hypothyroidism newborn screening

Based on
PPV

A

Based on high TSH

PPV 60-70%

152
Q

Cystic fibrosis affects which organs

Where is defect

Newborn dx

A

Lungs: recurrent infections
Pancreas: malabsorption, steatorrhoea, diabetes
Liver - cirrhosis

Transmembrane conductance regulator

High blood immune reactive trypsin

153
Q

What is MCADD

Newborn screening

A

Medium chain AcylCoA dehydrogenase
- Fatty acid oxidation disorder

No acetyl coA produced

  • needed for TCA cycle
  • needed for ketone production

Screening acylcarnitine levels by tandem MS
Cot death - go to sleep, can’t break down fat, dies of hypoglycaemia

154
Q

Homocystinuria presentation

A

IEM

Lens dislocation
Mental retardation
Thromboembolism

155
Q

Osmolarity equation

A

2(Na+K) + urea + glucose

156
Q

Anion gap formula

Normal anion gap

A

Na+K - Cl - bicarb

~14-18mmol/l

157
Q

T2DM dx

IGT

A

Fasting > or = 7mM
OGTT > or = 11.1

HbA1c: 6.5% (48)

Glucose tolerance test

  • 75g glucose given
  • Diabetes = >11.1mM at 2h
  • IGT = 7.8-11.1 at 2h (fasting <7)
158
Q

Body response to hypoglycaemia (normal)

A
  1. Insulin suppression
  2. Glucagon release
  3. Adrenaline release
  4. Release of cortisol

FFA undergo beta oxidation in mitochondria to provide energy (ketone by products) - ketones, FFAs and glucose increase

159
Q

Investigations in acute hypoglycaemia pt

A

Measure and confirm it is hypoglycaemia
Urine
ABG

Continuos glucose monitoring over 7 days when not acute

160
Q

Hypoglycaemia causes in diabetics

A

Medications

1) Oral hypoglycaemic
- Sulphonlyureas, Meglitinides (short acting sulfonylureas), GLP-1 agents (exanatides)
2) Insulin
- Rapid acting (with meals), long acting (hypos at night/between meals)
2) Other drugs
- beta blocker, salicyclates, alcohol

SGLT1 inhibitors can also make people hypoglycaemic

161
Q

Hypoglycaemia causes in non-diabetics

A 
Critically unwell
Organ failure
Hyperinsulinaemia
Post-gastric bypass
Extreme weight loss - anorexia with poor liver glycogen stores
162
Q

Blood tests to differentiate causes of hypoglycaemia

A 
Insulin 
C-peptide - marker of endogenous insulin - 
Drug screen
Auto-antibodies
Cortisol/GH
FFA, blood ketones
Lactate
163
Q

Hypoglycaemia with low insulin and low c-peptide causes

A

Appropriate response to hypoglycaemia

  • Fasting/starving
  • Strenuous exercise
  • Critically ill
  • Endocrine deficiencies : Hypopituirary, Adrenal failure
  • Liver failure - failure of glycogenesis and glycogenolysis
164
Q

Neonate hypoglycaemia causes

A

Pathological
If no ketones - IEM
- FFA raised, low ketones
- MCADD, FAOD, GSD type 1

If ketones - IEM

  • FFA raised, raised ketones
  • MSUD, GH deficiency, Galactosoaemia

Explainable

  • premature, co-morbidities, IUGR, SGA
  • Inadequate glycogen and fat stores
  • Should improve with feeding
165
Q

Hypoglycaemia, high insulin, high C-peptide

Next investigations

A

Sulphonylurea drug screen

  • If negative
  • Insulinoma (MEN1). Tx = resection
166
Q

Sulphonylureas mechanism of action

A

Bind to K+ channels and force them to close
–> Calcium entry

Insulin secretion independent of glucose

Normally: Glucose goes down glycolytic pathway, produced ATP, which closes K+ sensitive ATP channels
–> K+ can’t leave cell –> membrane depolarises and Calcium enters –> insulin secretion

167
Q

Hypoglycaemia, high insulin, low c-peptide cause

A

Factitious insulin usage

168
Q

Hypoglycaemia - persists with tx, undetectable insulin and C peptide, undetectable FFA and negative ketones

Cause

A

Non-islet cell tumour hypoglycaemia - mesenchymal/epithelial tumours
- Producing IGF-2 that binds to insulin receptor, switches off own insulin and ketones and FFAs not produced

169
Q

Hypokalaemia causes

A

1) Intestinal loss - D&V, fistula
2) Renal loss
- Mineralocorticoid excess (always in ectopic ACTH),
- Diuretic
- Renal tubular disease
- Conn’s (hyperaldosteronism)
- Osmotic diuresis (uncontrolled DM)

3) Redistribution - insulin, alkalosis

170
Q

What does zona fasiculata make?

A

Cortisol

Glucocorticoid

171
Q

Zona glomerulosa or fasiculata - which is thicker

A

Fasiculata - make more cortisol than aldosterone

172
Q 
Low T4 (<5)
High TSH (>50)
Dx
A

Primary hypothyroidism

173
Q

Primary hypothyroidism + Addisons =

A

Schmidt’s syndrome now called PGAS T2 (polyglandular autoimmune syndrome type 2)

174
Q

Test for Addison’s disease

A

Short Synacthen

  • measure cortisol and ACTH at start
  • give 250 microgram synthetic ACTH by IM
  • Check cortisol at 30 and 60 minutes

Addison’s ACTH>100, cortisol <10nM in both

175
Q

Glucose tolerance test used to diagnose what

A

Acromegaly

Diabetes

176
Q

Acromegaly test

A

Glucose tolerance test

  • Measure GH - in normal it will be suppressed
  • In acromegaly - GH fails to supppress
177
Q

HTN adrenal mass differentials

A

Phaeochromocytoma (tumour secreting adrenaline)
Conn’s syndrome (tumour secreting aldosterone)
Cushing’s syndrome secretes cortisol

178
Q

High urinary catecholamines
Dx
Management

A

Phaeochromocytoma

Urgent alpha blockade with phenoxybenzamine
Fluid with this so they don’t go into shock
Beta blocker next day (for reflex tachycardia)
Then arrange surgery

179
Q

What is a phaeochromocytoma

A

Adrenal medullary tumour that secretes adrenaline and can cause severe HTN, arrhythmia and death

180
Q

Phaeochromocytoma associations

A

MEN2
NF1
Von Hippel Lindau

181
Q

High sodium, low K, aldosterone raised, renin lowered

A

Primary hyperaldosteronism
aka Conn’s syndrome
Important to do test if HTN and young!!

182
Q

T2 DM obese F
HTN, bruising, high Na, low K+
Aldosterone low, renin low

A

Cushing’s syndrome

Conn’s excluded by aldosterone low

183
Q

Best tests for Cushing’s syndrome

A

Midnight cortisol (if asleep) high
- but can’t be done on someone that is ill as they will have a high cortisol
Dexamethasone is dynamic test
- cortisol not suppressed in Cushing’s syndrome

184
Q

Causes of Cushings

A

1) Steroids
2) Pituitary dependent Cushing’s disease (85%)
3) Ectopic ACTH
4) Adrenal adenoma

185
Q

Cushing’s syndrome on low dose dexamethasone test

- what’s next

A

Sample from pituitary (IPSS)

NOT high dose dexamethasone - as good as a guess

186
Q

Normal potassium

A

3.5-5mmol/L

187
Q

Which hormones regulate renal potassium

A

Angiotensin II

Aldosterone

188
Q

What stimulates aldosterone

A

ang-2

K+ high

189
Q

Aldosterone effect on Na conc

A

NONE

Na and water in

190
Q

Where dose aldosterone act

A

Principal cells in cortical collecting tubule

  • binds to mineralocorticoid receptor
  • expression of epithelial sodium channels
  • as sodium reabsorbed, lumen becomes -ve
  • k moves down electrical gradient
191
Q

Causes of hyperkalaemia

A

1) Excessive intake - oral, parenteral, stored blood transfusion

2) Transcellular movement
- Acidosis
- Rhabdomyolysis
- DKA (treakment with insulin will drop K)
- malfunctioning valves

3) Decreased excretion
- AKI (oliguric phase)
- CKD
- K sparing diuretics (spironolactone)
- Addison’s
- ACEi, ARBs, NSAIDs

Could also be delayed separation - delay in separating the cells in the blood sample from the serum, so some cells break down and release potassium, causing a falsely high potassium level

192
Q

Management of hyperkalamia

A

10ml 10% calcium gluconate
100ml 20% dextrose + 10 units insulin
Nebulized salbutamol
Tx underlying cause

193
Q

Hypokalaemia causes

A

1) GI loss/ low intake
- D+V
- Anorexia (+ laxative use)
- Fasting/diet

2) Renal loss
- In ascending LOH: loop diuretics/ Bartter syndrome
- In DCT: thiazide diuretic/Gitelman syndrome
- Hyperaldosteronism
- –> can be tumours, ectopic ACTH as cortisol binds to MR
- Osmotic diuresis

3) Redistribution into cells
- Insulin
- beta-agonists
- alkalosis

Rare: renal tubular acodosis 1 + 2, hypomagnesia

194
Q

Clinical features of hypokalaemia

A

muscle weakness
cardiac arrhythmia
polyuria, polydipsia (DI)

195
Q

Screening of hypokalaemia

A

Aldosterone:Renin ratio

For Conn’s

196
Q

Hypokalaemia management

A

Oral SandoK and monitor

If < 3
IV potassium chloride
Max rate 10mM/hr
- Rates higher irritate peripheral veins

Tx underlying cause

197
Q

Elevated TSH, Normal T4, TPO antibodies

A

Subclinical hypothyroidism with risk of later clinical hypothyroidism

198
Q

Tired

T4 normal, TSH normal

A

Euthyroid

199
Q

Low T4, High TSH

A

Primary hypothyroidism

200
Q

High thyroglobulin

A

Used to screen for recurrence of differentiated thyroid carcinoma

201
Q

High calcitonin

A

To screen for medullary thyroid carcinoma

202
Q

Pituitary hormones

controls

A 
GH - GHRH
Prolactin - TRH; Dopamine -ve 
ACTH - CRH
TSH - TRH
FH, LSH - GnRH
203
Q

Increased skull/head size, deafness, high otput cardiac failure, bone pain, microfractures

Biochem

A

Paget’s disease

Only ALP high

204
Q

Causes of primary hyperparathyroidism

A

90%: Parathyroid adenoma

Rest: Chief cell hyperplasia

205
Q

Aldosterone mechanism of action

A

binds to MR in cortical collecting tubes. Serum glucocorticoid kinase expressed, phosphorylates nedd4 (normally degrades sodium channels) -> sodium re absorption increased -> -ve lumen -> potassium moves down electrical gradient

Na conc not affected as water follows it

206
Q

Metabolic acidosis effect on K+

A

Hyperkalaemia

207
Q

Raised anion gap causes and cuttoff

A

> 18mmol/l

K: etocidosis
U: raemia (renal failure)
L: actic acidosis
T: oxins (ethylne glycol, methanol, paraldehyde, salicyclate)

208
Q

Liver functions

A 
Intermediary metabolism
Protein synthesis
Xenobiotic synthesis
Hormone metabolism
Bile synthesis
Reticulo-endothelial
209
Q

What is intermediay metabolism in liver

A 
Glycolysis 
Glycogen storage
Glucose synthesis
Amino acid synthesis
Fatty acid synthesis
Lipoprotein mtabolism
210
Q

Liver function tests

A

Synthetic function

  • Albumin
  • Clotting - PT
  • Glucose

Liver cell damage markers

  • ALT
  • AST
  • GGT
  • ALP
  • Bilirubin

AFP - tumour market

211
Q

Elevated AST/ALT ration

A

Suggestive of alcoholic liver disease or advanced fibrosis/cirrhosis in absence of alcohol use

Aspartate transaminase (AST) also raised in

  • HCC
  • Hepatitis
  • MI
  • Acute pancreatitis
  • AKI
212
Q

Elevated GGT

A

Chronic alcohol use

Also slightly up in bile duct disease and hepatic mets

213
Q

Markedly elevated ALP causes

A

Obstructive jaundice or bile duct damage

Less elevated in viral hepatitis or alcoholic liver disease
+ Bone disease (mets and pregnancy)

ALP is in high concentration in liver, bone, intestine and placenta
>5 x normal: Bone (Paget’s, osteomalacia), liver (cholestasis, cirrhosis)
<5 x normal: \bone (tumours, fractures, osteomyelitis), liver (infiltrative disease, hepatitis)

214
Q

Low albumin causes

A

Sepsis, shock - most common
Reduced production - chronic liver failure, malnutrition
Loss - kidney/ GI

215
Q

Alpha feto protein (AFP) elevation causes

A

HCC tumour marker

Pregnancy, testicular cancer

216
Q

Approach to jaundice (raised bilirubin)

A

Normal ezymes

  • Haemolysis
  • Gilbert’s

ALT/AST: hepatocellular

  • acute
  • Chronic

AST: Cholestatic

  • Dilated ducts = obstruction e.g. cancer, gallstones
  • Undilated ducts = drugs/PBC-PSC, pregnancy etc - do liver screen

Unconjugated vs conjugated v rarely measured clinically

217
Q

After US and abnormal LFTs, liver screen tests

A 
CK, TFTs, fasting lipids, fasting glucose
Hepatitis serology
Coeliac serology
Alpha-1-antitrypsin
Ceruloplsmin (<50y)
Liver AAbs (LKM, aSMA, AMA
Immunoglobulins
Ferriin
218
Q

Isolated ALT increase

A

Think fatty liver disease if 3 times norm (norm =40)

219
Q

Drug causing cholestasis

cholestasis LFTs

A

Augmentin

ALP markedly high

220
Q

Courvoisier’s sign

A

Painless palpable gall bladder, jaundice unlikely to be caused by gall stones

221
Q

ALT > 1000

A

Only 3 causes

1) Toxins (e.g. paracetamol)
2) Viruses
3) Ischaemia

222
Q

Endocrine risk if obstetric bleed

How to manage and prevent this risk

A

Pituitary infarction as big andslightly ischaemic in pregnancy
ALA Sheehan syndrome - loss of pituitary hormone function
- Tired - no ACTH or TSH
- normal BP
- No return of periods

Syntocinon, ergometrine and antibiotics

223
Q

Galactorrhoea - what nvestigation to do

A

Prolactin (>600 is high)
>6000 = prolactinoma

Should also do pituitary function testing

  • LHRGH, TRH, Hypoglycaemia
    • insulin for hypo (<2.2) increases CRF and GHRH
224
Q

Assessing pituitary function

A 
CPFT method
Fast overnight, IV access
0.15 units/kg insulin
200mcg TRH
100mc LHRH

Measure glucose, cortisol, GH, LH, FSH, TSH and prolactin every 30 mins
Normal - GH reaches 10, cortisol reaches 550, glucose <2.2 and then recovers after 30min

225
Q

Prolactinoma treatment

A

Bromocriptine or cabergoline

Dopamine agonist

226
Q

Acromegaly treatment

A

1) pituitary surgery - curative
2) radiotherapy
3) Cabergoline
4) Octreotide

227
Q

Hyponatraemia, hypokalaemia
Hypoglycaemia

Cause: WW = TB

A

Addison’s disease

Cause: WW = TB
Illness increases need for steroids

228
Q

Hyponatraemia, hypokalaemia
Hypoglycaemia

Primary hypothyroid

A

Schmidt’s syndrome - PGAS T2

229
Q

Addison’s disease signs and test

A

Hyponatraemia hyperkalaemia

Short synacthen test

  • measure acth and cortisol at beginning
  • 250mcg ACTH IM
  • check cortisol at 30 and 60mins

In Addison’s - cortisol <10 at both 30 and 60 mins

230
Q

Addison’s signs

A

Low BP/ postural hypotension
Pigmentation/tan

Fluids
Hydrocortisone
Thyroxine last

231
Q

Adrenal mass differential

A

Conn’s
Cushing’s
Pheo

232
Q

Cushing’s test

Give all even though not used anymore

A

Cortisol 12 midnight (don’t stop making in Cushing’s)
Dexamethasone suppression test - not suppressed in Cushing’s

Cushing’s Syndrome caused by an adrenal tumour/ ectopic ACTH

  • low dose: no change
  • high dose: NO CHANGE

Cushing’s Disease:

  • low dose: no change
  • high dose: NORMAL SUPPRESSION
233
Q

Conn’s what is it

Treatment

A

Primary hyperaldosteronism

Surgery - find tumour

234
Q

Cushing’s syndrome causes

A

Oral steroids
Pituitary dependent Cushing’s disease
Ectopic ACTH
Adrenal adenoma

235
Q

Cushing’s syndrome as cortisol not suppressed by dexamethasone

Next step

A

Sample from pituitary - majority pituitary

236
Q

What is porphyriasis

A

7 disorders caused by deficiency in enzymes, involved in haem biosynthesis —> build up of toxic haem precursors

237
Q

Acute intermittent porphyriasis type of inheritance and what is it

A

Porphriasis = group of disorders with deficiency of enzymes involved in haem biosynthesis so get build up of toxic haem precursors

AIP = deficiency of hydroxymethylbilane (HMB) synthase
Autosomal dominant

Neurovisceral symptoms only. No cutaneous manifestations
Dx ALA + PBG in urine (port wine urine)
Precipitated by ALA synthase inducers (steroids, ethanol, barbiturates), stress (infection,surgery), reduced calorie intake, premenstrual

Treatment - avoid precipitating factors, analgesia, IV carbonate/haem arginate

238
Q

What is acute porphyriasis with skin lesions

Inheritance

A

Hereditary coproporphyria (HCP) and Variegate porphyria (VP)

Autosomal dominant

Neurovisceral and skin lesions

Deficiency in corpoporyphrinogen oxidase or protoporphyrinogen oxidase
Raised porphyrins in faeces and urine

239
Q

Non-acuteporphyriasis type

A

Skin lesions only

CEP (congenital erythropoietic porphyria)
EPP (erythropoietic protoporphyria)
PCT (porphyriasis cutanea tarda)

EPP
Photosensitivity, burning, itching oedema after sun exposure
Deficiency in ferrochetelase

PCT
Inherited/acquired
Urophorphyrinogen decarbocxylqse deficiency
Cutaneous symptoms of vesicles on sun exposed sities
Dx: urinary uroporphyrins + coproporphyns + ferritin
Tx: avoid precipitants (alcohol, hepatic compromise, phlebotomy)

240
Q

Combined pituitary function test

Method

Results

Contraindications

A

Give insulin, GnRH, and TRH. Measure levels at 0, 30, 60, 90, 120 mins

1) insulin
— adequate cortisol response = > 170 to above 500nmol/l
— norm GH response = > 6mcg/l

2) TRH
— norm = TSH rise to >5 (30min > 60min)
Hyperthyroid = TSH remains suppressed
Hypothyroid = exaggerated response

3)GnRH
— norm = Peaks at 30 or 60 mins. LH > 10, FSH > 2

241
Q

Bloods findings in Addison’s disease

Examination findings

Test to do

Treatment

A

Hyponatraemia hyperkalaemia
Hypoglycaemia

Low BP, pigmentation

Short SynACTHen test
In Addison’s - cortisol < 10nM at 30 and 60 min

Treat with fluids (saline), hydrocortisone, then lastly thyroxine ?

242
Q

Adrenal mass differentials

A

Phaeo
Cushing’s syndrome
Conn’s syndrome

243
Q

Cushing’s test

Cushing’s causes

A

Dexamethasone test. In Cushing’s - cortisol is not suppressed
If high - sample from pituitary next

Most oral steroids
85% Cushing’s disease
Ectopic ACTH
Adrenal adenoma (10%)

244
Q

Vit A deficiency clinical picture

excess clinical picture

A

Deficiency = colour blindness

Excess = exfoliation hepatitis

245
Q

Vit D deficiency clinical picture

Excess clinical picture

A

Deficiency = osteomalacia/rickets

Excess = hypercalcaemia

246
Q

Vit E deficiency clinical picture

A

Deficiency = Anaemia, neuropathy, ? Malignancy, IHD

Excess = none

247
Q

Vitamin K deficiency clinical picture

Test

A

Defective clotting

PTT

248
Q

B1 deficiency

Clinical picture

Test

Management

A

Beri beri
Neuropathy
Wernicke syndrome

RBC transketolase

Replace thiamine. No test needed usually

249
Q

B2 deficiency clinical picture

A

Glossitis

250
Q

B6 deficiency clinical picture

Excess clinical picture

A 
B6 = pyridoxine
Deficiency = dermatitis / anaemia

Excess = neuropathy

251
Q

B12 deficiency clinical picture

A

Pernicious anaemia

Other autoimmune conditions - thyroid/T1DM

252
Q

Folate deficiency clinical picture

A

Macrocytic anaemia

Neural tube defects

253
Q

Niacin deficiency clinical picture

A

Diarrhoea, dementia, dermatitis and ultimately death

254
Q

Iodine deficiency clinical picture

A

Hypothyroid

255
Q

Fluoride deficiency clinical picture

Excess clinical picture

A

Dental caries

Fluorosis

256
Q

High amylasse

A

Acute pancreatitis - usually >10 x normal upper limit

Smaller increases in other acute abdomen states
Salivary isoenzyme also exists

257
Q

CK forms

A

MM- skeletal muscle
MB 1+2: Cardiac muscle
BB: Brain - activity minimal even in severe brain damage

258
Q

Raised CK causes

A

Rhabdomyolysis

Muscle damage due to any cause
Myophathy (DMD) - >10 x ULN
MI (>10 x ULN)
Severe exercise ( 3 x ULN)
Physiological - Afro Caribbean (<5x ULN)
259
Q

Dx criteria for MI biomarkers

A

Troponin typical risk and gradual fall (marker of choice for MI)
More rapid rise and fall of CK-MB

AST + LDH also raised

\+ At least one of:
Ischaemic symptoms
Pathological Q waves on ECG
ECG changes indicative of ischaemia
Coronary artery intervention
260
Q

HF biomarker

A

ANP

Best = Brain natriuretic peptide

261
Q

39yo F, BMI 43 has elevated ALP and RUQ pain. What other enzyme can you measure to confirm dx

A

GGT (gamma glutamyl transferase)

262
Q

Hypoglycaemia definition

A

<3.4mmol/L at imperial

263
Q

hypoglycaemia symptoms

A

Adrenergic - tremors, sweating, palpitations, hunger

Neuroglycopenic - Somnolence, confusion,inco-ordination, seizures, coma

Or none

264
Q

Which scan for bone density in hyperparathyroidism

A

Radius - DEXA

265
Q

Which scan for bone density in steroid exposure?

A

hip and back and also for post-menopausal osteoporosis

DEXA

266
Q

LVH causes

A

HTN

Aortic stenosis

267
Q

ST elevation in leads II, III, aVF
Diagnosis
Which part of heart affected

A

Inferior wall MI

Supplied by RCA

268
Q

drug that inhibits the enzyme dipeptidyl dipeptidase IV (DPP-4)

A

Gliptins

269
Q

MEN syndromes

A

MEN1: pituitary, parathyroid, pancreas

MEN2a: parathyroid, phaeo, medullary thyroid
MEN2b: phaeo, medullary thyroid, mucosal

270
Q

Check for recurrence of papillary thyroid cancer

A

Thryoglobulin

271
Q

Hyperthyroid causes

Treatment

A

Graves
Toxic multinodular Goitre
Single adenoma

Lower uptake on scan
Thyroiditis
Post patrum thryoiditis

Others
Silent/facticous thyrodititis
TSH induced
Thyroid cancer induced

Dx by low TSH, high T3/4, Tch sncan, antibodies

Beta block if >100 HR
Radioiodine. Only if not working:
Carbimazole, propylthiouracil as rare risks of agranuolcytosis

272
Q

Types of thyroid cancer

Treatment

A

Papillary (>60%) - psammoma bodies
Follicular
Medullary (Men 2A) - calcitonin producing. Originates in parafollicular cells

Surgery +/- Radioiodine
+ Thyroxine (to reduce TSH)

273
Q

Hypothyroid causes

A

Hashimoto’s (TPO antibodies)
Atrophic
Post Surgery/radioiodine
Drugs - lithium, amiodarone

274
Q

Thyroid phsyiology

A

Iodide uptake into thyroid actively
TPO coverts back to iodine
TG takes up iodine and converts to thyroxine (2 iodone form DIT and eventually thyroxine)

T4 stored in thyroid gland.

All controlled by TSH

275
Q

Thyroxine in periphery

A

T4

TBG-T4 75%
TBPA-T4 20%
Albumin-T4 - 5%
fT4 0.03%

276
Q

Troponin after MI

A

Rises 4-6h post MI
Peaks 12-24h post MI
Remains elevated for 3-10 days

277
Q

Why might TPMT be measured

A

Prior to azathioprine use

278
Q

Hyperammonia newborn red flags for the condition

A

Condition = Urea cycle disorder (in liver to detoxify ammonia)

Vom, no diarrhoea
Resp alkalosis
Hyperammonia - v toxic. 1 day exposure = coma + IQ shutdown
Neurological encephalopathy

Rx: Stop feeds, 10% dextrose
Get rid of ammonia with sodium benzylate or sodium phenylacetate
Dialyse

279
Q 
Newborn with
Vomitin + Diarrhoea
Conj hyperbilirubinaemia
Hepatomegaly
Hypoglycaemia
SEPSIS
A

Galactosaemia = carbohydrate disorder

280
Q

Cholesterol absorption

A

Diet (EGGS) but Comes mainly from bile.
Transported across intestine by NPC1L1 (ABC G5/8 are reverse). Bile reabsorbed in ileum

In liver, downregulates HMG coAr eductase
(-ve feedback)
2 paths for cholesterol in liver
1) Hydrolysed into bile acids
2) Esterified by ACAT and with TG and apoB incorporated into VLDLs (MTP control)

CETP mediates

  • Cholesterol from HDL to VLDL
  • TG from VLDL to HDL

ABC 1A mediates
- HDL pick up of excess peripheral cholesterol

LDL transports cholesterol to periphery

281
Q

Triglyceride transport and metabolism

A

Source = fatty foods that are hydrolysed and broken into fatty acids
Fatty acids resynthesised to TG and taken up by chylomicron
Chylomicrons are hydrolysed to FFAs
FFAs taken up by liver and adipose tissue

Liver resynthesises FFAs into TG and exports to VLDL

282
Q

Primary hypercholesterolaemia
Mutations

Presentation
Management

A

Dominant mutations of LDL receptor
(Or apoB, PCSK9 genes)
- coronary disease risk 10x increased

Homozygote: Arcus, atheroma of aortic root <20yo
Hetrozygote: Arcus later, xanthelasma, tendon xanthelasma

PCSK9 function is to bind LDL receptor and degrade
Gain of function mutation = LDL receptor degraded –> high LDL

Evolocumab (PCSK9 mAb)

283
Q

Diabetes treatment

A

Start with metformin
Then GLP-1 analogue (Exanatide)
or basal insulin

If long standing poorly controlled T2DM with heart disease
consider:
- Empaglaflozin
- Liraglutide (GLP-1 analogue)

GLP-1 secreted from gut and signals pancreas to make insulin

Empagliflozin = SGT2 inhibitor = makes you pee out protein

284
Q

Primary hypertriglyceridaemia

A

1: lipoprotein lipase deficiency or apoC II deficiency
- eruptive xanthomas
- Cream floats to top of plasma

IV: Increased TG synthesis
- Cream doesn’t float to top but get VLDL

V: More severe version of type IV
- Mix of chylomicrons and VLDL on plasma test

285
Q

A 60-year-old woman with hypothyroidism presents with progressive dyspnoea and tiredness. FBC reveals macrocytic anaemia.

A

Probably B12 deficiency because autoimmune

Check parietal cell antibodies

286
Q

Albumin levels vary with

A

Posture and so does renin

  • Rises in the upright position.
  • Some people have so-called benign postural and/or exercise-induced albuminuria.
287
Q

Digoxin toxicity features

A

Arrhythmia: the most common arrhythmias are ventricular extrasystoles, ventricular bigeminy / trigeminy and atrial tachycardia with complete heart block

Anorexia, nausea and vomiting and occasionally, diarrhoea

Confusion especially in the elderly

Yellow vision (xanthopsia), blurred vision and photophobia

Symptoms of under-treatment and toxicity may be similar

288
Q

Lipid soluble drug metabolism by the liver

A

1) Oxidation by cytochrome p450

2) Conjugation by sulphate/gluconaride

289
Q

Lithium levels are affected by

A

Any diuretics
NSAIDS
ACEi/ARBs

Dehydration

290
Q

Substance missuse

Cyanide poisoning presentation
Heroin overuse presentation
Aspirin (salicyclate)
Ecstasy

A

Dead - brick red and almond smelling

Heroine: ARMED - C: Respiratory depression. +ve 6MAM urine test

Aspirin: Metabolic acidosis, repiratory alkalosis late presentation. Haeomodialyse

Ecstasy: Wide dilated pupils, agitated

TCAs: Wide dilated pupils, drowsiness, hyperreflexia, widened QRS

291
Q

Activated charcoal use

A

Generally if within an hour of taking

Not for use in poisoning with cyanide, iron, ethanol, lithium, acid or alkali, pesticides

292
Q

How to assess long term drug use

Best quick and cheap test for drug use

A

Hair sample

Saliva

293
Q

A 65 year old female presents to her new GP 5 years after an operation on her abdomen. She cannot remember the details of the operation but does remember that she was suffering from severe Cushing’s Disease at the time. She now notes a progressive ‘tanning’ of the skin

A

Nelson Syndrome
Old days, patients who had pituitary Cushing’s had bilateral adrenalectomy as a treatment option. This would
leave the pituitary adenoma free to grow, and the ACTH would continue to rise. In addition POMC levels (precursor to ACTH) would rise too. This would make patients become more tanned.

The pituitary tumour would get larger, and eventually cause real local problems, originally described by Nelson

294
Q

A 27 year old woman presents with a three month history of weight gain, deepening voice and secondary amenorrhoea. Examination reveals clitoromegaly, acne, greasy skin and hirsutism. Serum cortisol is grossly elevated and ACTH levels are undetectable.

A

Adrenal carcinoma because primary hyperaldosteronism

295
Q

CAH

A

21-Hydroxylase Deficiency is most common cause (CYP21)

Diagnosis: High 17-Hydroxyprogesterone in serum
Hyponatreamia with Hyperkalaemia

Path (6 decks)

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