Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 5 MEDICINE Pathology > Chemical Pathology > Flashcards

Chemical Pathology Flashcards

1
Q

Osteoporosis

A

Loss of bone mass, normal calcium/biochemistry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Osteomalacia/rickets

A

Vitamin D deficiency cause:

1. Osteomalacia - low Ca AND phosphate, raised ALP!! Looser zones. An also be caused by renal failure due to no vitamin D.

2. Rockets - widened epiphyses at wrist, Costochondral swelling, myopathy. Can be caused by anticonvulsants which break vitamin D down.

*phytic acid can also cause vitamin D deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pagets

A

leg!
spine, hip, skull

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Hypocalcemia/hypercalcemia

A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Equation for calculating corrected calcium?

A

Total serum calcium + (0.02 x (40 - serum albumin) )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Role of PTH in kidney?

A

Converts 25 to 1-25OH (calcitriol). Via 1-alpha hydroxylase

Note 25 is stored and measured form. It is made in liver by 25 hydroxyalse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Vitamin D2 vs D3

A

Ergocalciferol - plant
Cholecalciferol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Parathyroid bone disease

A

oteitis fibrosa cystica - seen in primary hyperparathyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Renal osteodystrophy

A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pthrp?

A

Made in pregnancy, mother sacrifices calcium to build fetus skeleton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which hormone controls water balance?

A

ADH, acts on V2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Stimuli for ADH release?

A

Reduction in blood volume or pressure - sensed by baroreceptors
Increased osmolality sensed by osmoreceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

first step in the clinical assessment of a patient with hyponatraemia?

A

Assess volume status

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hypovolemic hyponatremia signs?
Causes?
Management?

A

- Tachycardia
–Postural hypotension
–Dry mucous membranes
–Reduced skin turgor
–Confusion/drowsiness
–Reduced urine output
–Low urine Na+ (<20) = KEY!! - most reliable, send test

1. Diuretics
2. Diarrhea, vomiting
3. Salt losing nephropathy

0.9% saline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Euvolemic hyponatremia
causes?
Management?

A

Hypothyroidism - TFTs
•Adrenal insufficiency - short syncthathen test
•Syndrome of inappropriate ADH (SIADH) - plasma and urine osmolality

Fluid restriction, check underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hypervolemic hyponatremia signs?
causes?
Management?

A

Raised JVP
–Bibasal crackles (on chest examination)
–Peripheral oedema


Cardiac failure

–Cirrhosis

–Renal failure eg nephrotic syndrome,

Fluid restriction
–Treat the underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Hyponatremia?
Pathogensis?

A

Serum sodium < 135 mmol/L
Excess water due to ADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

SIADH causes?
Diagnosis?
Management

A

CNS or lung pathology, Drugs (SSRI, TCA, opiates, PPIs, carbamazepine), surgery

•Reduced plasma osmolality AND
•Increased urine osmolality (>100) = KEY
Tests rule out other causes of hypothyroidism, adrenal insufficiency AND hyPOVolemic hyponatremia are important

Demeclocycline
Tolvaptan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Central pontine myelenosos symptoms? Cause?

A

quadriplegia, dysarthria, dysphgia, seizures, coma, death

Raising sodium too much

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Hypernatremia
Causes?
Management?

A

Serum [Na+] > 145 mmol/L

GI losses, sweat, diabetes insipidus!!

Correct water deficit - 5% dextrose

•Correct extracellular fluid volume depletion - 0.9% saline

•Serial Na+ measurements - Every 4-6 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Severe hyponatremia

A

Low GCS, siezures
Treat with 3% hypertonic saline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Investigations in patient with diabetes insipidus?

A

Serum glucose (exclude diabetes mellitus)
–Serum potassium (exclude hypokalaemia)
–Serum calcium (exclude hypercalcaemia)
–Plasma & urine osmolality
–Water deprivation test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Are thiazide diuretics useful in patients with high bp and a history of CAD?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How many years of poor glucose control before symptoms

A

15 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Benefits of SGLT2 inhibitors eg empagliflozin

A

Additionally Beneficial in HF and patients w nephropathy

Flozins also useful in CKD with patients w or without type 2 diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

GLP1- analogues

A

1. Exanatide
2. Liraglutide
3. Semaglutide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

T2DM management

A

1. Metformin
If insufficient best to combine with SGLT2 or GLP1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Adrenal glands and what is made in each zone

A

GFR = salt (aldosterone), sugar (cortisol), sex (comes last)

in medulla = adrenaline and NA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Learn reference range for sodium potassium and urea
Hemoglobin wbc and platelets

A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Addison’s disease
Confirmatory test?

A

Short Synacthen test
You inject them with it
Normal patients - rise in cortisol
Addison’s - No rise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Phaeochromocytoma management

A

Alpha blocker first
Beta blocker next
Surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Conns syndrome management? (Primary hyperaldosteronism)

A

Spirinolactone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Top causes of Cushing’s syndrome?

A

Top cause is being on steroids

Then Pituitary dependent cushings disease = 85%
Ectopic ACTH
Adrenal Adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Cushing’s syndrome if low dose dexamethasone suppresses cortisol falls to LESs than 50, what is diagnosis?

A

Normal obese person

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

If a patients cortisol remains high after a low dose dex suppression, what is the next test you need to do?

A

ACTH
you need to know if it suppressed
If ACTH is suppressed = adrenal tumour causing cushings - then the next test would be adrenal ct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

If a low dose dex fails to suppress, what test do you do?

A

Pituitary sampling
High dose dex test is now redundant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

hypercalcemia
symptoms?
causes?
management?

A

Polyuria / polydipsia
Constipation
Neuro – confusion / seizures / coma

1. primary hyperparathyroidism - PTH high. parathyroid adenoma, associated with MEN1
2. Malignancy - pTH suppressed. bony mets, haematological malignancy, small cell lung cancer
3. other minor like sarcoidosis


management = fluids, bisphosphonate ONLY if malignant cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Hypocalcemia

symptoms - neuromuscular excitability

causes

A

Non-PTH driven:

1. vitamin D deficiency – dietary, malabsorption,

2. chronic kidney disease (1α hydroxylation)**

3. PTH resistance (“pseudohypoparathyroidism”)

Due to low PTH:
1.Surgical (inc post thyroidectomy)
2. Auto-immune hypoparathyroidism
3.Congenital absence of parathyroids (eg DiGeorge syndrome)
4. Mg deficiency (PTH regulation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Osteitis fibrosa is seen in?

Renal osteodystrophy is seen in?

A

1. primary hyperparathyroidism
2. secondary hyperparathyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

pagets disease

A

raised ALK PHOS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

interpret arterial blood gas results

A

H+ ] 35-45 nmol/l in ECF

pH 7.35 -7.46

pH = log 1/ [H+ ]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

acid buffers in the body?

A

bicarbonate - main
hemoglobin - main in rbcs
phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

metabolic acidosis presents as?
causes

A

H+ increased or HCO3- decreased

compensated = reduction in CO2

Increased H+ production e.g. diabetic ketoacidosis
2. Decreased H+ excretion e.g. Renal tubular acidosis
3. Bicarbonate loss e.g. intestinal fistula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

respiratory acidosis presents as?

A

increased CO2 which causes high H+

poor ventilation - pulmonary emboli
impaired gas exchange - emphysema

compensated = kidney increasing bicarb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

metabolic alkalosis presents as?
causes?

A

decreased H+, increased HCO3-

compensation = increased CO2

Increased H+ production e.g. diabetic ketoacidosis
2. Decreased H+ excretion e.g. Renal tubular acidosis
3. Bicarbonate loss e.g. intestinal fistula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

respiratory alkalosis presents as?

A

low CO2, which causes low H+ and bicarb

hyperventilation

compensation = decreases H+ excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

A

1. H+/pH tells us whether there is an overt acidosis or alkalosis - look at this first
2. then this - pCO2 tells us whether there is a respiratory disturbance (primary or secondary)
3. then pO2
4. then Bicarbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

sensitivity of test?

A

people in who disease is present

true positive/total disease present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

specificity of a test?

A

people in who disease is absent
True negative/total disease absent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

positive predictive value?

negative predictive value?

A

true positive/all positive

true negative/total negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

metabolic diseases & newborn screening

A

PKU
homocystinuria - lens dislocation, thromboembolism, mental retardation
MCAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

urea cycle defect presentation

A

hyperammonemia = KEY finding!
when levels very high -> coma
long term psychiatric findings may occur
red flags =
1. vomiting without diarrhea
2. neurological encephalopathy
3. avoidance food/ change in diet
4. resp alkalosis, hyperammonemia

autosomal recessive except OTC which is

treatment = removal of ammonia eg with sodium benzoate, dialysis sometimes

low protein diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

organic acidurias findings?

A

hyperammonemia with metabolic ACIDOSIS (contrast to urea cycle disorder)

in neonates:
1. unusual odour, lethargy, truncal hypotonia + limb hypertonia
2. hyperammonemia with metabolic ACIDOSIS
3. hypocaclemia, neutropenia, thrombopenia

chronic intermittent form in older kids:
- ketoacidotic coma, reyes syndrome (child with reyes syndrome can be due to metabolic disease -> therefore run ammonia, amino acid, organic acid, glucose and lactate tests)


- involve metabolism of branch chained amino acids leucine, isoleucine, valine
3OH-isovaleric acid - excretion causes cheesy sweaty smell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

MCAD findings?

A

HYPOKETOTIC (cant break down fat) HYPOGLYCEMIA -> key finding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Galactosemia (carb disorder)
presentation?

A

Conjugated hyperbilirunemia!!!
vomiting, diarrhea
hypoglycemia
sepsis
bilateral cataracts -> due to galctitiol buildiup in kids if not picked up earlier

galactose-1-phoshate uridyl transferase (Gal-1-PUT) is the most severe and the most common

diagnosis = Red cell Gal-1-PUT

galactose free diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Glycogen storage disease type 1 (von gierke)
a carb disorder

A

Hypoglycemia!!!
lactic acidosis!!!

hepatomegaly
nephromegaly
neutropenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

mitochondrial disorders examples?

Tests?

A

Barth (cardiomyopathy, neutropenia, myopathy)
MELAS (mitochondrial encephalopathy, lactic acids and stroke-like episodes)
Kearns-Sayre (Chronic progressive external ophthalmoplegia, retinopathy, deafness, ataxia)

lactate - elevated fasting lactate is a clue
CK
CSF protein
muscle biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

peroxisomal disorders?
presentation?

A

impaired metabolism of very long chain fatty acids

neonates = severe hypotonia
infants = retinopathy often leading to early blindness, sensorineural deafness, hepatic dysfunction, osteopenia and enlarged fontanelle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

lysosomal storage disease?

A

intraorganelle substrate accumulation leading to organomegaly -> connective tissue, solid organs, bone, cartilage -> dysmorphia, regression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

common problems in LBW babies?

A

respiratory distress syndrome, retinopathy of prematurity

intraventricular hemorrhage

patent ductus arteriosus

necrotising enterocolitis - necrosis of bowel wall = abdominal distension (AXR Shows intramural air), bloody stools

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

differences in a nephron in a baby

A

short proximal tubule -> reduced resorptive capacity
short loops of henle and dct -> reduced urine concentrating ability

distal tubule quite unresponsive to aldosterone -> persistent loss of sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

drugs given to babies

A

bicarbonate for acidosis
caffeine/theophiline for apneoa of prematurity
indomethacin for pda

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Hypernatremia in newborns?

A

common in first days of life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Hyponatremia in newborns?

A

congenital adrenal hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

treatment for hyperbilirubenemia

A

in a term baby:
340 = phototherapy
450 = exchange transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

causes of hyperbilrubinemia in first few days of life?

A

Haemolytic disease (ABO, rhesus etc)
G-6-PD deficiency
Crigler-Najjar syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

causes of prolonged jaundice?jaundice that lasts for more than 14 days in term babies and more than 21 days in preterm babies

A

Prenatal infection/sepsis/hepatitis
Hypothyroidism
Breast milk jaundice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

conjugated!!! hyperbilirubinemia is always pathological. causes include?

A

- biliary atresia
- choledocal cyst
- ascending cholangitis in total parenteral nutrition in premature babies due to lipid content
-inherited metabolic disorders eg galactosemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

the lower limit for hypocalcemia is much lower in in infants than in adults.

A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Osteopenia of prematurity presents as?
treatment?

A

fraying, splaying, cuffing of long bones
low phosphate -> suggest calcium depletion even though calcium may be normal
Alk Phos 10x upper limit of normal

calcium and phosphate supplements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

rickets present as?

A

osteopenia due to vitamin D deficiency
frontal bossing, bow legs

hypocalcemic seizure/ cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what is porphyria?

A

deficiencies in heam synthesis pathway

Neurovisceral symptoms - due to 5 ALA
blistering cutaneous symptoms. - due to porphoryins
non blistering cutaneous symptoms - due to porphoryins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

most common porphyria?

A

1. Porphyria cutanea tarda - uroporphyrinogen decarboxylase deficient. skin affected only, non acute. sun avoidance is treatment. typically caused by liver disease eg hep b
2. Acute intermittent Porphyria
3. Erythorpoietic protoporphyria - most common in children. skin affected only, non acute. sun avoidance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

ALA synthase deficiency causes?

A

x-linked sideroblastic anemia

not a porphyria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

PBG synthase/ALA dehydratase deficiency signs?

A

- decreased PBG
- ALA accumulation = neurovisceral symptoms = coma, motor neuropathy, abdominal pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

HMB synthase/PBG deaminase deficiency signs?

A

causes Acute intermittent prophyria

-increased PBG and, ALA = neurovisceral symptoms - siezures, quadraparesis.
SIADH

no cutaneous syndromes as no increase in prophoryins

90% people have no symptoms only which precipitating factors eg ALA synthase inducers/drugs

diagnosis = increased urinary PBG/ALA

treatment = IV heam arginate, IV carbs, avoid precipitants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

name the acute porphyrias with skin lesions and the deficient enzymes

A

Hereditary coproporphyria - coproporphyrinogen oxidase
Variegate porphyria - protoporphyrinogen oxidase


neurovisceral symptoms due to accumulated products which inhibit HMB synthase by negative feedback

blistering skin lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

how to differentiate acute porphyrias

A

AIP – no skin lesions
HCP & VP – skin lesions

Urine PBG – raised in all three
Urine and faeces for porphyrins
Raised HCP or VP, but not AIP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

how to test for porphyrias

A

neurovisceral symptoms:
1. Urine PBG
-normal = excludes attack
- raised = enzyme activity, urine/faecal porphyrins, DNA

Skin features:
- urine/faecal porphyrins

photosensitivity (cutaneous syndrome without blisters):
- red cell protoporphyrins to rule out EPP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Urine samples taken during an acute attack for diagnosis of porphyrias should be?

A

protected from light

81
Q

primary hypercholesterolemia causes

A

familial hypercholesterolemia type 2 - homozygous may have atheroma of aortic root, heterozygote = corneal arcus, xanthelasma, tendon xanthoma

polygenic hypercholesterolemia

familal hyperalipoproteinemia

phytosterolemia

82
Q

Most common mutation in Familial hypercholesterolemia (type 1 familial dyslipidemia)

A

1. Mutation of LDL gene
2. mutation of APOB

least common = gain of function mutation in PCSK9

83
Q

primary hypertryglyceridemia causes ?
presentations?

A

type 1 familial dyslipidemia (hyperchylomicronemia) = lipoprotein lipase or apoC 2 deficiency. creamy layer on top of plasma sample which indicates chylomicrons. eruptive xanthomas.

type 4 familial dyslipedemia (hypertriglyceridemia) = increased synthesis of TG. Vldl particles which dont float

type 5 familial dyslipedemia =apoA 5 deficiency. vldl + layer of floating chylomicrons

84
Q

name a cause of primary mixed hyperlipedemia and its cause

A

familial dysbetalipoproteinemia type 3 = ApoE 2 polymorphism = palmar straie (yellow palmar crease), eruptive xanthomas on elbow

85
Q

state 3 secondary causes of hyperlipedemia

A

metabolic - obesity, gout, diabetes - could present with eruptive xanthomas
renal dysfunction
obstructive liver disease - eg primary billiary cirrhosis - may cause gross xanthelasma
hormonal factors - hypothyroidism

86
Q

hypolipidemia causes

A

AB - lipoprotenemia = MTP deficiency
Hypo - B -lipoprotenemia = truncated ApoB
Tangier disease - HDL deficiency

87
Q

Obesity treatment?

A

diet and execise
orlistat
Bariatric surgery if BMI > 40 kg/m2 - with gastric band being least invasive

88
Q

which enzyme controls uptake of idoide into thyroid gland?

A

TSH
once taken in, idoide converted to iodine (by thyroid peroxidase)
iodine taken up by thyroglobulin
Tyrosine residues iodinated (blocked by thionamides)
iodotyrosines join to form thyroxine

89
Q

what is T4 mostly bound to?

A

1. TBG - 75% thyroglobulin binding globulin
2. TBPA
3. Albumin

90
Q

3 most common causes of hypothyroidism?

A

1. hashimotos disease
2. Atrophic thyroid - congenital or acquired
3. Post Graves disease - eg radioiodine treatment

others less common


if thyroid peroxidase antibodies present, this suggests autoimmune cause of hypothyroidism
hypothyrodism is linked to other autoimmune processes so measure adrenal antibodies, early morning cortisol

91
Q

effect of giving too much levothyroxine?

A

osteopenia, atrial fibrillation

92
Q

what is subclinical hypothyroidism? learn!

A

T4 levels are normal
pituitary gland senses this as too low, thus TSH levels are elevated
+TPO antibodies predicts later thyroid disease!!

only treat if cholesterol levels are elevated

93
Q

what happens in early pregnancy?

A

hcg produced binds to TSH receptor, causes increased T4. and lower TSH
later on in pregnancy when hcg decreased, T4 decreases and TSH increases
normal pregnancy physiology

94
Q

what is sick euthyroid syndrome? learn!

A

low T4 level
TSH normal or slightly high
T3 low

individual sick eg sepsis, thyroid shuts down to reduce metabolic rate

- can be mistaken for hypothyroidsim or subclinical hypothyroidism -> to differentiate these patients wont have clinical signs of hypothyroidism - bradycardia, hyporeflexia, weight gain

95
Q

3 main causes of hyperthyroidism?

A

1. Graves disease
2. Toxic multinodular goitre
3. single Toxic adenoma
these 3 have high uptake on technetium scan

others: postpartum thyroiditis, subacute thyroiditis (these 2 have low uptake on scan)

96
Q

thyrotoxicosis/ hyperthyroidism management

A

- B block if pulse >100
think of other autoimmune conditions might have
- ECG - to rule out a fib
- DEXA scan - rule out osteopenia
- radioactive iodine -> release radiation to destroy thyroid gland -> may precipitate thyroid storm. AVOID in patient with Graves eye disease
- carbimazole/propylthiouracil (thionamides, prevent iodide to iodine)

presence of thyroid autoantibodies can help with diagnosis

97
Q

treatment for viral or portpartum thyroiditis?

A

thyroxine replacement
contrast to other causes of hyperthyroidism

98
Q

Thyroid cancer types?
treatment?

A

1. papillary thyroid cancer
2. follicular thyroid cancer
3. medullary thyroid cancer

thyroidectomy, then radioiodine treatment to remove any remaining thyroid cells, then excess thyroxine to lower TSH levels to prevent thyroid cells growth

measure thyroglobulin in plasma to check if functioning thyroid tissue still present

99
Q

how to screen for medullary thyroid carcinoma?

A

measure calcitonin and CEA

(mtc is associated with MEN2)

99
Q

if a patient presents with elevated thyroglobulin? what does this mean@

A

you need to screen for recurrence of differentiated thyroid carcinoma

100
Q

pituitary driven thyrotoxicosis presents as?

A

elevated TSH and T4

101
Q

Map out the purine catabolism pathway

A

Purine -> hypoxanthine

Hypoxanthine -> xanthine
Via xanthine oxidase

Xanthine -> urate
Via xanthine oxidase

Urate -> allantoin
Via uricase

Uricase is inactive in humans, so urate must be excreted. And it is insoluble. Men have higher urate plasma concs.

102
Q

Learn
-> de Novo purine synthesis
-> Purine salvage pathway - more efficient, dominates, except in bone marrow

A

103
Q

What is the rate limiting step in de novo purine synthesis?

A

PRPS -> PPRP
catalysed by PAT

Inhibited by feedback inhibition by the products AMP and GMP

104
Q

Importance of HGPRT?

A

Transfers guanine back up to GMP
And hypoxanthine back up to ionosinic acid

105
Q

Lesch Nyhan syndrome cause?
Symptoms?

A

HGPRT deficiency. No GMP and IMP being made through salvage pathway, decreased negative feedback on PAT, so increased de novo purine synthesis which is catabolised to urate

X linked
Normal at birth
Developmental delay apparent by 6 months
Hyperuricemia!! -> gouty arthritis in child
Choreiform movements
Mental retardation
Self mutilation - > bite lips, digits

106
Q

Secondary causes of increased urate production?

Lesch nyhan is a primary cause

A

Conditions with increased cell turnover:

-> myeloproliferative disorders
-> lymphoproliferative disorders

107
Q

Causes of decreased urate excretion?

A

Primary = FJHN

Secondary = CRF, lead poisoning, diuretics!! barters syndrome

108
Q

Acute gout is called?
Chronic gout is called?

A

Podagra

Tophaceous

109
Q

Hyperuricemia management?

A

Acute gout attack - NSAIDs, colchicine

Non acute/ interval - water, reduce synthesis with allopurinol, probenacid

110
Q

Side effects of allopurinol?

A

Interacts with azathioprine

Causes levels of mercaptopurine to build up. Mercaptopuribe metabolises azathiprine this u are doubling/increasing azathioprine dose to toxic amount which can break down bone Marrow -neutropenia

111
Q

Allopurinol mechanism of action?

A

Lowers urate levels by inhibiting xanthine oxidase

112
Q

Gout mono sodium urate crystal shape

A

Needle shaped and Negatively birrefringente

(It is blue at 90 degrees to axis/ compensator)

113
Q

Pseudo gout

A

Caused by pyrosphosphate crystals
Positively birrefringent so they are blue parallel to axis/compensator

Commonly affects people with osteoarthritis, commonly affects knee

114
Q

vitamin A deficiency and excess?

A

vision problems

skin problems, hepatitis

115
Q

Vitamin E deficiency?

A

anemia
neuropathy

116
Q

vitamin K deficiency?

A

defective clotting
PTT test

117
Q

vitamin B1/thiamine deficiency?
test?

A

beri beri
neuropathy
wernicke syndrome


RBC transketolase

118
Q

Vitamin B2/ riboflavin Deficiency?
test?

A

glossitis

RBC glutathione reductase

119
Q

Vitamin B6/pyridoxine deficiency?
test?

A

dermatitis/anemia

excess = neuropathy

RBC AST activation test

120
Q

B12 Cobalamin deficiency?
test?

A

pernicious anemia

serum B12

121
Q

niacin deficiency?

A

pellagra - diarrhea, dermatitis, dementia

122
Q

iodine deficiency can cause?

A

goitre
hypothyroidsm

123
Q

zinc deficiency can cause?

A

dermatitis

124
Q

copper deficiency can cause?
excess?

A

anemia
wilsons disease

125
Q

fluoride deficiency can cause?

A

dental caries

126
Q

leptin vs ghrelin?

A

ghrelin - hunger hormone
leptin - anti hunger hormone

PYY - satiety hormone

127
Q

interpreting BMI

A

25 - 30 is overweight
> 30 is obese
> 40 is morbidly

128
Q

what waist circumference increases risk of CV disease?

A

men >94
women > 80 cm

waist circumference important in measuring degreeof adiposity and CVR risk

129
Q

polyunsaturated fat is good because it lowers?

A

LDL

130
Q

treatment for obesity?

A

exclude endocrine cause
exclude complications of obesity
educate
diet and exercise
medical therapy - orlistat, GLP-1 agonist
surgical therapy

131
Q

what surgery is the best for obesity

A

gastric bypass - you loose the most weight with this specific type as well

132
Q

benefits of bariatric surgery?

A

improvement in T2DM
improvement in HTN
improved lipid profile
resolution of PCOS and improved fertility

133
Q

marasmus vs kwashiokor

A

kwashiokor patients lack protein only and they are edematous

marasmus low carbs and lipids as well, muscle wasting

134
Q

best predictor of MI risk and benefit of statins?

A

measurement of total plasma cholesterol and lipoprotein levels

135
Q

alcohol intoxication treatment?

A

thaimine pabrinex

136
Q

what type of autoimmune disease is primary billiary cirrhosis?

A

organ specific but no organ specific antibodies

137
Q

SLE symptoms

A

skin - butterfly rash, photosensitivity, discoid lupus
oral ulcers
joints
neurological - psychosis, depression
serositis - pleuritic chest pain
renal - lupus nephritis - 6 classes - 1 presentation is wire looping = thick walled capillaries in GBM = KEY!!

hematological - pancytopenia
immunological - ANA, anti-dsDNA, antiSmith (most specific but not specific), antiHistone(drug related lupus eg hydralazine)

non infective endocarditis -> libman-sacks

138
Q

scleroderma/ systemic sclerosis
diffuse vs limited form

A

excess collagen

diffuse= antibodies to DNA topoisomerase Scl70. truncal skin involvement

Limited = CREST anticentromere antibody
Calcinosis
raynauds
esophageal dysmotility
sclerodactyly
Telangiectasia

nucleolar pattern of immunofluorescence may be seen
nail fold capillary dilatation may be seen
microstomia

Histology; Intimal proliferation, leading to renal hypertensive crisis - KEY

139
Q

mixed connective tissue disease presents as ?

A

features of:
SLE
Scleroderma
Polymyositis - elevated CK
Dermatomyositis - gottrons papules

Speckled pattern of ANA seen
anti-RNP

140
Q

Sarcoidosis presentation?

A

joint
skin - lupus pernio, erythema nodosum
lungs - BHL, fibrosis, lymphocytosis
lymphadenopathy


heart
eyes -uveitis, keratoconjuctivitis
neuro - meningitis, cranial nerve lesions
liver - hepatitis, cholestasis, cirrhosis

bilateral enlargement of parotids


hypercalcemia
Hypergammaglobinemia
Raised ACE

141
Q

state 2 large vessel vasculitis

A

Giant cell arteritis - steroids, ESR bloods, biopsy
Takayasu arteritis

142
Q

State 2 medium vessel vasculitis

A

polyarteritis nodosa - renal and mesenteric vessels - gut ischemia, renal impairment, angiogram shows beading of vessels due to aneurysms, associated with hep B. necrotising arteritis

kawasaki disease - fever, erythema and desquamation of palms and soles, lymphadenopathy, self limiting although coronary arteries may be affected

143
Q

state 2 small vessel vasculitis
describe their presentations?

A

Wegners - granulomatosis with polyangiitis:
1. ENT - nosebleeds, sinusitis, ear problems
2. Lungs - breathlessness, cavities in lungs
3. Kidneys - blood/protein in urine
- C ANCA +ve <- request this. antibody binds to proteinase 3 in CYTOPLASM

Churg strauss - eosinophilic granulomatosis with polyangitis
1. Asthma
2. Eosinophilia
3. Vasculitis
- P ANCA against myleoperoxidase, binds Perinuclear. <- request this test

144
Q

a palpable purpural rash is due to?

A

Vasculitis

145
Q

secondary causes of vasculitis

A

infective endocarditis
Rheumatoid arthritis
SLE

146
Q

ethylene glycol poisoning signs

A

alcoholic
calcium oxalate stones

146
Q

imaging choice for 28 year old with suspected renal stones

A

CT over ultrasound KUB

146
Q

causes of pre renal AKI

A

True volume depletion
Hypotension
Oedematous states
Selective renal ischaemia
Drugs affecting glomerular blood flow

147
Q

Intrinsic/Renal AKI

A

Vascular Disease e.g. vasculitis
Glomerular Disease e.g. glomerulonephritis
Tubular Disease e.g. ATN
Interstitial Disease e.g. analgesic nephropathy

contrasts, drugs, endogenous toxins

infiltration - amyloidosis, lymphoma
immune dysfunction - vasculitis

148
Q

dilated bilateral kidneys on ultrasound may be caused by?

A

BPH

149
Q

Post Renal AKI causes

A

Hallmark is physical obstruction to urine flow

(Intra-renal obstruction)
Ureteric obstruction (bilateral)
Prostatic / Urethral obstruction
Blocked urinary catheter

150
Q

most common causes of AKI?

A

decreased renal perfusion
medication
contrast media
postoperative
sepsis

151
Q

causes of CKD?

A

Diabetes
Atherosclerotic renal disease
Hypertension
Chronic Glomerulonephritis
Infective or obstructive uropathy
Polycystic kidney disease

152
Q

consequences of CKD?

A

Progressive failure of homeostatic function
-Acidosis
-Hyperkalaemia

2]Progressive failure of hormonal function
-Anaemia
-Renal Bone Disease - Osteitis fibrosa, Osteomalacia, Adynamic bone disease, Mixed osteodystrophy

3]Cardiovascular disease - MOST IMPORTANT consequence of CKD main cause of death. risk directly predicted by EGFR
-Vascular calcification
-Uraemic cardiomyopathy -Left ventricle (LV) hypertrophy, LV dilatation, LV dysfunction

4]Uraemia and Death

153
Q

What two measures do we use to define severity of acute kidney injury?

A

1. serum creatinine
2. urine output

154
Q

contraindications to renal transplantation?

A

active sepsis
any malignant disease

155
Q

osteitis fibrosa

A

Osteoclastic resorption of calcified bone and replacement by fibrous tissue

156
Q

what is adynamic bone disease?

A

Excessive suppression of PTH results in low turnover and reduced osteoid

157
Q

treatment for renal bone disease?

A

Phosphate control
Dietary
Phosphate binders

Vit D receptor activators
1-alpha calcidol
Paricalcitol

Direct PTH suppression
Cinacalcet

158
Q

heroin abuse main risks?

A

respiratory depression, aspiration pneumonitis

159
Q

cocaine abuse main risks?

A

cardiac dysarrhythmias, MI, acute HF, sudden death

160
Q

amphetamines main risks?

A

hyperthermia, rhabdomyolysis, renal failure

161
Q

methadone main risks?

A

respiratory depression

162
Q

pregabalin/gabapentin main risks?

A

euphoria

163
Q

how to calculate osmolality?

osmolality = charged molecules + uncharged


= cations + anions + urea + glucose

= Na, K. + Cl, HCO3. + urea + glucose
since charged molecules = uncharged, what is the simplified formula

A

2 (Na+ K+) + urea + glucose


you double sodium and potassium because cations = anions (cl- and hco3-)


very high osmolality can cause someone to be unconsious due to dehydration

in diabetes would be due to hyperosmolar hyperglycemic syndrome

164
Q

how to calculate anion gap?

(cations - anions )

what is a normal anion gap?

A

Na + K - Cl - bicarb

4-12?

if high anion gap eg 50, it means cl and bicarb are low and thus other anions making up their space - may be ketones, alcohol, lactate (metformin overdose can cause lactic acidosis)

165
Q

learn normal ph and C02 range so you can tell if something is acidosis or alkalosis in exam and metabolic vs repsiratory

A

166
Q

definition of type 2 diabetes

A

fasting glucose > 7

if fasting glucose is below 7 but
GTT shows plasma glucose >11.1 at 2 hours

2 hour value 7.8 - 11.1 = impaired glucose tolerance

167
Q

causes of mixed alkalosis and acidosis?

A

aspirin overdose

168
Q

Potts fracture vs Colles fracture

A

Potts -> ankle

Colles -> wrist

169
Q

single investigation to distinguish cause of hypercalcemia between cancer, primary hyperparathyroidism and sarcoidosis

A

PTH

in primary hyperparathyroidism, PTH is raised or inappropriately normal

in sarcoidosis, PTH is suppressed. sarcoidosis is treated with steroids

170
Q

hypercalcemia symptoms?

A

psychic moans (depression), bones (fractured - cystic lesions, brown tumour on histology), groans(abdo pain, pancreatitis), stones(renal)

nephrogenic DI -> polydipsia, polyuria


renal stones(pain, hematuria), pancreatitis, Peptic ulcer disease

band keratopathy

171
Q

**hypercalcemia commonly presents with depression

A

172
Q

emergency management of hypercalcemia?

A

Ca2+ >3.0 mmol/L = emergency management:
0.9% saline:
furosemide
IV pamidronate

non emergency:
hydration
avoid thiazides
surgery - parathyroidectomy

173
Q

aldosterone effect in kidney?

A

stimulates sodium reabsorption and increases urinary potassium excretion

174
Q

state 3 main causes of hyperkalemia

A

1. renal impairment (reduction in GFR)
2. drugs: ACE inhibitor, angiotensin 2 receptor blocker, spironolactone, NSAIDS
3. low aldosterone: Addisons, Type 4 RTA which has low renin and low aldosterone
4. release from cells: rhabdomyolysis, acidosis

175
Q

management for hyperkalemia?

A

10 ml 10% calcium gluconate
50 ml 50% dextrose + 10 units of insulin
Nebulized salbutamol
Treat the underlying cause

176
Q

causes of hypokalemia

A

GI loss

Renal loss
Hyperaldosteronism, (Excess cortisol)
Increased sodium delivery to distal nephron
Osmotic diuresis - thiazide and loop diuretic

Redistribution into the cells
Insulin, beta-agonists, alkalosis

Rare causes: Renal tubular acidosis type 1& 2 (barterr in ascending loop and gietlemann syndromes in dct), hypomagnesaemia

177
Q

hypokalemia symptoms?

A

Muscle Weakness
Cardiac arrhythmia
Polyuria & polydipsia (nephrogenic DI)

178
Q

hypokalemia management?

A

Serum potassium 3.0-3.5 mmol/L
Oral potassium chloride (two SandoK tablets tds for 48 hrs)
Recheck serum potassium

Serum potassium < 3.0 mmol/L
IV potassium chloride
Maximum rate 10 mmol per hour

179
Q

What screening test would you order in a patient with hypokalaemia and hypertension?

A

aldosterone:renin ratio

180
Q

normal potassium levels?

A

3 -5 mmol/L

181
Q

gold standard way of demonstrating hypoglycemia?

A

venous blood glucose

182
Q

c peptide is a cleavage product of what

A

proinsulin

183
Q

hypoglycemia from injected insulin causes what c peptide levels

A

low cpeptide

high insulin

184
Q

name a cause of hypoinsulineamic hyperglycemia

(low insulin
low c peptide)

A

anorexia (low liver gylcogen stores)
critically unwell
fasting
endocrinopathies - addisons disease, pahypopituitarism

185
Q

name a cause of hyperinsulineamic hyperglycemia

(high insulin
high cpeptide)

A

pancreatic causes - insulinoma, sulphunylureas

186
Q

hypoglycemia, low cpeptide low insulin BUT also negative ketones and FFA in

1. 60 year old man
2. newborn


typically due to?

A

60 year old - non-islet cell tumour hypoglycemia

newborn - errors of fatty acid metabolism

187
Q

define Km

A

1/2vmax

188
Q

causes of raised ALP?

A

intrahepatic and extrahepatic bile ducts
bone causes - fracture, pagets disease, cancer etc
placenta - pregnancy in last trimester, germ cell tumours
Intestine


- check LFTS - GGT ALT, if normal check vitamin D

189
Q

patient presents with polydipsia, polyuria, glycosuria. diabetes suspected. very dehydrated. BP 80/40 patient unconcious - what is the most likely reason?

patients anion gap is 12, is diabetic ketoacidosis likely?

A

hyperosmolar non ketotic coma

not DKA due to low anion gap

190
Q

ectopic acth -> lung cancer -> resp exam shows reduced sounds on right, dullness to percussion, increased vocal resonance

most likely cause?

A

collapse and consolidation

191
Q

how to distinguish acute renal failure from chronic renal failure?

A

renal biopsy

192
Q

pituitary failure causes hypotension. true or false?

A

False!!

- pituitary gland does not control aldosterone! it controls cortisol!
- renin controls aldosterone

193
Q

what investigation is done next when someone is found to have prolactinoma on pituitary mri??

A

combined pituitary function test!! -ACTH, GH

(make sure pituitary can respond to stress)
done by administering insulin to cause hypoglycemia

severe hypoglycemia occurs? -> 20% dextrose

194
Q

In pituitary failure, what hormone is most important to replace first?


in addition to various hormones replaced hydrocortison, thyroxine, estrogen GH, what other treatment is needed for prolactinoma?

A

hydrocortisone

fludrocortisone is given in addisons disese! = adrenal!! failure (aldosterone replacement)

cabergoline or bromocriptine!! (dopamine agonist)

195
Q

pituitary tumour, prolactin <3000
other hormones low
most likely diagnosis?

A

non functioning pituitary adenoma

196
Q

28 year old with visual field defect
GH quite high other hormones low. most likely diagnosis?

A

acromegaly!

Year 5 MEDICINE Pathology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions