3) GI system 2 + endocrinology Flashcards

Question 1

Q

ACHALASIA

- what is it? describe the pathology?

Answer

A

= degeneration of myenteric plexus → impaired func of oesophageal smooth muscle and failure of lower oesophageal sphincter (LOS) to relax → a functional stenosis or oesophageal stricture → ↓motility and dysphagia

Question 2

Q

ACHALASIA:

initial symptoms? 3
late symptoms / signs? 2

Answer

A

Dysphagia
– solids > fluids (most common feature)

Regurgitation (80%) and Reflux

Chest pain
– Sub-sternal or retrosternal cramping

Late signs

nocturnal cough
aspiration of reflux (pneumonia)

Question 3

Q

ACHALASIA:

most serious DDx to consider?
red flags that may indicate this?

Answer

A

oesophageal or mediastinal cancer

Weight loss
loss of appetite
fatigue
haematemesis
Supraclavicular node

→ urgent endoscopy (not barium enema)

Question 4

Q

ACHALASIA:

distinctive sign on barium swallow? 1
gold-standard test? 1

Answer

A

oesophageal dilatation followed by stricture at lower oesophageal sphincter (BIRD BEAK SIGN)

nb aka rat tail sign (I think more accurate)

manometry = gold-standard

Question 5

Q

GASTRITIS:

most comon causes? 4
symptoms? 3

Answer

A

alcohol
NSAIDs
H.pylori
reflux / hiatus hernia

Question 6

Q

ALARMS symptoms which are red flags for more serious aetiology than gastritis? 6

Answer

A

Anaemia

Loss of weight

Anorexia

Recent onset or progressive symptoms

Melaena or Haematemesis

Swallowing difficulty (dysphagia)

also new onset over 50!

Question 7

Q

GASTRITIS:

test if suspect H.Pylori cause?
investigation if suspect more serious pathology / redf flags? 1

Answer

A

H.Pylori test – carbon-13 urea breath test or stool Ag

For breath test, must stop PPI/H2 antagonist 2wks before, as it gives false –ve

Endoscopy + Biopsy if red flags
– stop PPI/H2 antagonist 2 wks prior due to false –ve

Question 8

Q

GASTRITIS:

management if H. Pylori-induced?
management if not H Pylori induced? 2

Answer

A

H. Pylori = triple therapy
- 2 abx, 1 PPI

If NOT h pylori

stop nsaids / alcohol
PPI for 8 weeks

Question 9

Q

CHRONIC PANCREATITIS:

what is it?
most common causes? 2

Answer

A

Irreversible inflammation of the pancreas. Precise pathophysiology unknown, thought to be related to decreased HCO3- excretion → activation of pancreatic enzymes → tissue necrosis.

alcohol
gallstones (or tumour) obstruction

also other causes of acute pancreatitis (get repeated acute attacks which can -> chronic

Question 10

Q

CHRONIC PANCREATITIS:

main two symptoms?
symptoms / signs if exocrine mainly affected? 2
symptoms if endocrine mainly affected/ 3

Answer

A

EPIGASTRIC PAIN bores through to back
– Relieved on sitting forward +/- hot water bottle on epigastrium
- Worse 15-30 mins post-meal

NAUSEA + VOMITING +/- Anorexia

Exocrine – Malabsorption (bloating, steatorrhoea)

Endocrine – Diabetes mellitus (polyuria, polydipsia, fatigue, etc.)

Question 11

Q

CHRONIC PANCREATITIS:

bloods to do? (and findings)
findings on USS and CT scans? 1

Answer

A

FBC, U&Es, LFTs, CRP, ↑Glucose (DM), HbA1C,
↑Amylase, ↑Lipase

nb lipase and amylase may not be massively raised if chronic

Endo-USS (∆) – calcification, irregular duct walls, dilatation or cysts
CT (∆) – may show calcifications, atrophy, ductal dilatation
^basically CALCIFICATIONS!!!

Question 12

Q

CHRONIC PANCREATITIS:

diet modification? 2
mainstay of medical management? 3
possible indications for surgery? 3
prognosis?

Answer

A

1 – Diet Modification: ↓alcohol; ↓fat intake

2 – Medication

ANALGESIA – Up WHO pain ladder +/- Coeliac Plexus Block

ENZYME replacement – e.g. CREON (lipase)

INSULIN – for diabetes (complication)

nb also ?Octreotide – Somatostatin analogue

3 – Surgery
Indications – persistent pain, narcotic abuse, weight loss
Pancreatectomy/Pancreaticojejunostomy

Question 13

Q

SUBPHRENIC ABSCESS

what is it?
what two things is it normally caused by / secondary to? 2

Answer

A

localised collections of pus underneath the right or left hemi-diaphragm

norm occurs secondary to:

1) generalised PERITONITIS
- eg acute appendicitis, perf peptic ulcer, perf GB

2) BOWEL SURGERY

Question 14

Q

SUBPHRENIC ABSCESS

describe the clinical presentation?
what is the timescale of the onset of presentation with respect to timeline of cause?

Answer

A

Typically a pt. that develops features of toxicity 2-21 days after initial recovery from peritonitis OR operation!!

Swinging fever/pyrexia
Malaise, Nausea and Weight loss
Abdominal tenderness in subcostal region

± Upper abdo pain radiating to shoulder tip

± Dyspnoea (indicates lobe collapse or development of pleural effusion)

Question 15

Q

What can be seen on a CXR of a person with a subphrenic abscess?

other imaging done?

Answer

A

CXR – high diaphragm on affected side, gas or fluid under diaphragm, ± pleural effusion or lobe collapse

also do a CT scan (to visualise location of pus)

nb WCC often > 20,000

Question 16

Q

LIVER ABSCESS

what is it?
most common group of causative organisms in the UK? 1
most common group of causative organisms worldwide? 1

(can give examples of specific organisms)

Answer

A

localised collections of pus in liver caused by bacterial, parasitic or fungal organisms

UK = norm bacterial cause

Usually Klebsiella or E.Coli (adult), S.Aureus (child)

worldwide = norm amoebic cause

Question 17

Q

LIVER ABSCESS

localised symptoms + signs? 2
systemic symptoms? 5

Answer

A

RUQ Pain + Tenderness → radiates to R shoulder
Hepatomegaly + Abdo mass
SWINGING pyrexia + Night sweats
Nausea, Vomiting
Anorexia, Weight loss
Cough + dyspnoea – due to diaphragmatic irritation

± Jaundice

Question 18

Q

PYOGENIC (ie bacterial) LIVER ABSCESS

most common cause of pyogenic abscesses? (not organism but cause)
other causes?
broad principles of management?

Answer

A

Secondary to infection of abdo

ascending cholangitis (most common!)
diverticulitis
appendicitis
CD
PUD

Can be complication of liver biopsy or blocked biliary stent also endocarditis and dental infection

Usually Klebsiella or E.Coli (adult), S.Aureus (child)

management = antibiotics AND ct/uss-guided percutaneous drainage

^ most pts won’t respond to Abx alone!

Question 19

Q

AMOEBIC ABSCESS

norm causative organism?
what to ask in history in british patients to assess risk?
broad principles of management?

Answer

A

Entamoeba Histolytica – common in tropical areas w/ poor sanitation or overcrowding

Faecal-oral transmission, check travel Hx

ANTIBIOTICS – Metronidazole (1st line)

95% pts. respond to Abx (if really large may need drainage!)

Question 20

Q

What’s more common: primary liver tumours or liver metasteses from other primaries?

two main primary liver cancers? 2

most common tumour types which metastasise to the liver? 3

Answer

A

liver mets a lot more common that primary liver tumours

Hepatocellular carcinoma (most common primary 90%)
Choangio-carcinoma (2nd most common primary 10%)

mets from

lung
breast
GI tract (incl stomach)

Question 21

Q

risk factors for hepatocellular carcinoma:

lifetyle? 1
medical conditions (2 more common causes, 3 rarer causes)

Answer

A

= alcohol

= Viral hepatitis (C > B)
= primary biliary cirrhosis

haemochromatosis
A1-anti-trypsin deficiency
diabetes mellitus

Question 22

Q

CHOLANGIOCARCINOMA

most common cause? 1
what are findings of LFTs?
management?

Answer

A

PRIMARY SCLEROSING CHOLANGITIS (associated with UC)

nb also Flukes and N-nitrosasmines

obstructive picture on LFTs (higher ALP than others)

nb CEA is also often raised (though not specific)

surgical resection

Question 23

Q

Presentation of primary liver tumours:

localised signs / symptoms? 3
systemic signs / symptoms? 3

Answer

A

Often presents late with features of cirrhosis and decompensated chronic liver disease (DCLD)

RUQ pain (due to liver capsule stretch)
Hepatomegaly – ± mass and/or bruits
Splenomegaly
Fever, malaise
anorexia, ↓weight
Jaundice + Pruritis (Late = HCC; Early = CholangioCa)

Question 24

Q

HEPATOCELLULAR CARCINOMA:

what tumour marker to do?
what other specific blood tests to do? 2 (excl LFTs)
what investigation to AVOID? 1
management?

Answer

A

↑AFP (80% of HCC)

nb if +ve must check for testicular Ca

Heb B and C serology!

Liver biopsy – use with CAUTION, as it seeds tumour cells through resection plane

surgical resection

Question 25

Q

EPIGASTRIC HERNIA

location?
what herniates through where?
risk factors?
management options? 2

Answer

A

pass through linea alba above the umbilicus

normally fat herniates through abdo muscle (occasionally a bit of bowel if really large)

risk factors are same as any other hernia (eg obesity, heavy lifting, chronic cough etc)

watch and wait OR surgery

Question 26

Q

COLONIC POLYPOSIS

what does polyposis actually mean?
what condition does this most characteristically occur in? 1
other conditions it can occur in?

Answer

A

polyposis = numerous polyps in the bowel

FAP (familial adenomatous polyposis)

nb this is almost always asymptomatic!! and is only found if FHx of colon ca at early age or many polyps found on colonoscopy done for another reason!

can also occur in crohns / ulcerative colitis and other rarer genetic conditions

nb these include: (DON’T LEARN THESE!) - MUTYH-associated polyposis (MAP)

juvenile polyposis syndrome
Peutz-Jeghers syndrome
serrated polyposis syndrome.

Question 27

Q

FAP (familial adenomatous polyposis)

inheritance pattern?
common age of colon cancer?
monitoring provided to people found to have?
prophylactic management options?

Answer

A

autosomal dominant

40years norm age of cancer if not managed

regular colonoscopies from teenage years

have suspicous polyps removed during colonoscopies OR whole / part of large bowel resected prophylactically!

(nb similar to prophylactic mastectomy for BRCA genes)

Question 28

Q

Presentation of primary liver tumours:

localised signs / symptoms? 3
systemic signs / symptoms? 3

Answer

A

Often presents late with features of cirrhosis and decompensated chronic liver disease (DCLD)

RUQ pain (due to liver capsule stretch)
Hepatomegaly – ± mass and/or bruits
Splenomegaly
Fever, malaise
anorexia, ↓weight
Jaundice + Pruritis (Late = HCC; Early = CholangioCa)

Question 29

Q

HEPATOCELLULAR CARCINOMA:

what tumour marker to do?
what other specific blood tests to do? 2 (excl LFTs)
what investigation to AVOID? 1
management?

Answer

A

↑AFP (80% of HCC)

nb if +ve must check for testicular Ca

Heb B and C serology!

Liver biopsy – use with CAUTION, as it seeds tumour cells through resection plane

surgical resection

Question 30

Q

ANAL cancer DDx? 5

Answer

A

perianal warts
leukoplakia
lichen sclerosis
bowen’s disease
crohn’s disease

Question 31

Q

FAP (familial adenomatous polyposis)

inheritance pattern?
common age of colon cancer?
monitoring provided to people found to have?
prophylactic management options?

Answer

A

autosomal dominant

40years norm age of cancer if not managed

regular colonoscopies from teenage years

have suspicous polyps removed during colonoscopies OR whole / part of large bowel resected prophylactically!

(nb similar to prophylactic mastectomy for BRCA genes)

Question 32

Q

PERIANAL HAEMATOMA

- management options? 2

Answer

A

leave to resolve spontaneously

OR

evacuated under local anaesthetic

Question 33

Q

ANAL cancer

- symptoms? 6

Answer

A

bleeding
pain
altered bowel habit
pruritis ani
masses
strictures

Question 34

Q

ANAL cancer DDx? 5

Answer

A

perianal warts
leukoplakia
lichen sclerosis
bowen’s disease
crohn’s disease

Question 35

Q

FISTULA-IN-ANO

two types? (categorised by location)
management of each type?

Answer

A

nb always drain internal abscess if still present

Fistulotomy + Excision for both types but slightly different methods

HIGH fistula
- ie involving continence musles of anus
– requires ‘seton suture’ tightened over time to maintain continence

LOW fistula
- ie not involving muscles of continence
– fistulotomy and laid open to heal by secondary intention

Question 36

Q

REFEEDING SYNDROME

briefly describe pathophysiology (incl main ion/electrolyte involved!)
groups of pts most at risk? 5

Answer

A

in starved state: body metabolises protein + fat (subsequent drop in circulating insulin)

catabolic state also depletes intra-cellular phosphate (but serum levels norm)

when start refeeding: insulin incrteases which increases cellular uptake of phosphate -> LOW SERUM levels of PHOSPHATE (hypophosphataemia) -> symptoms / features of syndrome

malignancy
post-GI surgery
anorexia nervosa
starvation
alcoholism

Question 37

Q

REFEEDING SYNDROME

- symptoms / features?

Answer

A

HYPO-PHOSPHAETEMIC state norm occurs within 4 hrs

->

rhabdomyolysis
red + white cell dysfunction
respiratory insufficiency
arrythmias
cardiogenic shock
seizures
sudden death

Question 38

Q

REFEEDING SYNDROME

management? 2 (2 things to do, 1 group of things to monitor)
other health professional to be involved?

Answer

A

refeed SLOWLY

oral or IV phosphate if complications do occur (or low serum levels)

monitor bloods closely (glucose, lipids, Na, K, phosphate, Ca2+, Mg, zinc)

involve nutritionist

Question 39

Q

define these terms:

dysphagia
odynophagia
globus
dyspepsia

Answer

A

dysphagia = difficulty swallowing

odynophagia = painful swallowing

globus = sensation of lump in the throat

dyspepsia = indigestion (ie upper abdo fullness, heartburn, nausea, belching, or upper abdo pain)

Question 40

Q

REFEEDING SYNDROME

briefly describe pathophysiology (incl main ion involved!)
groups of pts most at risk? 5

Answer

A

in starved state: body metabolises protein + fat (subsequent drop in circulating insulin)

catabolic state also depletes intra-cellular phosphate (but serum levels norm)

when start refeeding: insulin incrteases which increases cellular uptake of phosphate -> LOW SERUM levels of PHOSPHATE (hypophosphataemia) -> symptoms / features of syndrome

malignancy
post-GI surgery
anorexia nervosa
starvation
alcoholism

Question 41

Q

REFEEDING SYNDROME

- symptoms / features?

Question 42

Q

If someone presents with weight loss, what do you want to ask them about as a part of a systems review:

systemic (my acronym)? 6
psych? 3
neuro? 4
diet / recreational drugs? 3
haematological? 4
resp? 3
cardiovascular? 4
GI? 10
urinary? 5
genital? 3
MSK / RHEUM? 1

Answer

A

SYSTEMIC (“AW FS FIN”)

appetite
weight loss
fatigue
sleep changes
fever
itch / rashes (any skin changes / lesions)
night sweats

PSYCH (“above head”)

mood
stress
body image

NEURO (“head”)

headache
visual changes
sensory loss
muscle weakness

DIET (“put in mouth”)

change to diet
polydipsia (DM)
recreational drugs (eg cannabis, ritalin)

HAEM (“lymph nodes”)

lumps neck, under armpits, groin
bruising
repeated infections
pale (anaemia)

RESP (“lungs”)

cough
haemoptysis
SOB

CARDIOVASCULAR (“heart”)

palpitations
light-headedness / syncope
chest pain
leg swelling

GI SYSTEM (mouth to anus)

mouth ulcers
dysphagia
dyspepsia / heart burn
vomiting
haematemesis
abdominal pain
bloating
jaundice
change in bowel habits (new IBS >50)
blood or pus per rectum

URINARY SYSTEM (kidneys, bladder)

flank pain
pain on passing urine
incontinence
polyuria (DM)
haematuria (kidney/bladder Ca)

GENITALS

breast lumps (or new lumps anywhere tbh)
testicular lumps
non-menstrual PV bleeding

MSK / RHEUM (“knees”)
- joint pain / swelling or stiffness

basically if someone presents just with weight kloss - do a full systems review until you find some positives then focus in on those (taking into account risk factors etc)

Question 43

Q

DYSPHAGIA:
- meaning?

DIFFERENTIAL DIAGNOSES:

mechanical cause? (1 malignant, 2 benign strictures, 3 external pressure, 1 other)
motility disorders? 4
other? 2

Answer

A

difficulty swallowing (either solids or fluids)

MECHANICAL CAUSE

= Oesophageal Ca (or gastric/pharyngeal)

oesophageal web or ring
= peptic stricture (from repeated reflux)

= lung Ca
= mediastyinal lymph nodes
- retrosternal goitre
- aortic aneurysm

pharyngeal pouch

MOTILITY DISORDERS
= achalasia
= diffuse oesophageal spasm
- systemic sclerosis (/CREST)
- neurological bulbar palsy*

OTHER

oesophagitis (reflux or candida/HSV)
globus (techincally not true dysphagia)

*nb bulbar palsy can be caused by many things incl parkinsons, chagas, myasthenia gravis

Question 44

Q

DYSPHAGIA:

with the answer to each one of these questions which dysphagia causes are you making more or less likely:

1) Was there (a) difficulty swallowing solids AND liquids from the start OR (b) was solids difficulty first and now both? (divides between 2 main groups of causes)
2) Is it difficult to make the swallowing movement? (if yes, makes 1 cause more likely)
3) is swallowing painful (odynophagia)? (if yes, makes 3 more likely)
4) is the dysphagia intermittent OR is it constant + getting worse? (1 for each)
5) does the neck bulge or gurgle on swallowing?

Answer

A

1) Was there (a) difficulty swallowing solids AND liquids from the start OR (b) was solids difficult first and now both?
- both first = motility cause (achalasia, CNS)
- solids first = stricture (benign or amlignant)

2) Is it difficult to make the swallowing movement?
- yes = bulbar palsy (esp if pt coughs on ‘swallowing’)

3) is swallowing painful (odynophagia)?
- yes
= oesophageal ulcer (benign or malignant)
= candida (immunocompromised or steroid INH)
= Oesophageal spasm

4) is the dysphagia intermittent OR is it constant + getting worse?
- intermittent = oesophageal spasm
- constant + worsening = malignant stricture

5) does the neck bulge or gurgle on swallowing?
- yes = suspect pharyngeal pouch

Question 45

Q

What two systemic conditions should you look for if have a pt with dysphagia (one is single condition, one is group of conditions)

Answer

A

1) systemic sclerosis

2) CNS disease
- eg parkinsons, myasthenia gravis etc

Question 46

Q

DYSPHAGIA:

why would you do an FBC, U+E and CXR on someone presenting with dysphagia? 3
two other 1st line interventions for dysphagia? 2

Answer

A

FBC (anaemia for Ca)
U+E (dehydration)

CXR (mediastinal enlargement, lung Ca)

1) Upper GI endoscopy + biopsy
2) barium swallow

Question 47

Q

DYSPEPSIA

- featuress of dyspepsis? (4 symptoms, 1 sign)

Answer

A

EPIGASTRIC PAIN
- related to hunger, specific foods or time of day

+/- BLOATING

FULLNESS after meals

HEARTBURN (retrosternal pain + reflux)

TENDER EPIGASTRIUM

Question 48

Q

DYSPEPSIA
- differential diagnoses? 5

what other groups of causes should you rule out? 3 (esp if epigatric pain predominant symptom)

Answer

A

gastric malignancy
duodenal / peptic ulcer (PUD)
gastritis (h pylori, nsaids, alcohol)
functional (non-ulcer) dyspepsia
oesphagitis / GORD

nb PUD norm occurs after prolonged gastritis

IF EPIGATRIC PAIN, also remember:

CARDIAC causes (eg ACS)
RESP causes (eg PE, pneumonia)
OTHER GI causes (eg pancreatitis, gall bladder)

Question 49

Q

DYSPEPSIA

- associated symptoms to ask about? (6, mneumonic)

Answer

A

ALARMS symptoms

A = Anaemia
L = Loss of weight
A = Anorexia
R = recent onset / progressive symptoms
M = Meleana / haematemesis
S = Swallowing difficulty (dysphagia)

Question 50

Q

DYSPEPSIA:

which pts would you send for urgent endoscopy?
1st line management / trial by treatment to do for other pts? 3 (+how long to try for)
what to do if no improvement after this time?

Answer

A

urgent endoscopy

1) new onset >50 years
2) any ALARMS features

INITIAL

1) STOP DRUGS causes dyspepsia (NSAIDs)
2) LIFESTYLE advice (reduce alcohol + smoking, big meals etc, weight loss)
3) OVER-THE-COUNTER ANTACIDS

try for FOUR WEEKS

IF NO IMPROVEMENT:

test for H Pylori

if positive = triple therapy
if negative = 4 wk PPI (then review)

then if continued symptoms after eradication or 4wks of PPI then consider endoscopy

Question 51

Q

FAECAL INCIONTINENCE

- three groups of causes 3 (give at least one example for each)

Answer

A

cause is often MULTIFACTORIAL!!!

1) SPHINCTER DYSFUNCTION
= vaginal delivery (tears or pudendal nerve damage)
- any surgical trauma to sphincter (following procedures for fistulas, haemorrhoids, fissures)

2) IMPAIRED SENSATION
= any spinal cord lesion 
= diabetes
= MS
= dementia

3) FAECAL IMPACTION
= overflow diarrhoea (v common in elderly)

nb although there is often no clear cause found, esp in elderly women, is norm multifactorial

Question 52

Q

FAECAL INCONTINENCE
- two body systems to examine? 2 (incl add on test)

when is faecal incontinence a red flag? what for?

Answer

A

1) ABDO exam
2) NEURO exam

incl DRE!!!

stool / contents of rectum
peri-anal sensation
rectal tone

ACUTE faecal incontinence = always consider CAUDA EQUINA / cord compression
- esp if neuro deficitis!

Question 53

Q

RECTAL BLEEDING:
- what % are caused by UPPER GI bleeds?

LOWER GI causes? 8

this is FRESH rectal bleeding (ie not meleana)

Answer

A

15% of rectal bleeding has upper GI source

diverticulitis
crohn’s / UC
colorectal cancer
some infectious gasrtoenteritis (eg campylobacter, shigella, salmonella, e coli., amoebas)
ischaemic colitis
mesenteric ischaemia
haemorrhoids
other perianal disease (fistula, fissure)

Question 54

Q

Most common cause of meleana?

Answer

A

UPPER GI bleed

Question 55

Q

difference between mesenteric ischaemia and ischaermic colitis?

describe difference in pathology and clinical presentation

Answer

A

MESENTERIC ISCHAEMIA

typically small bowel
due to embolism (AF is risk)
sudden onset, severe symptoms (abdo pain severe, out of keeping with exam findings)
lactic acidosis
urgent surgery
high mortality

ISCHAEMIC COLITIS

large bowel
multifactorial
acute but transient compromise in the blood flow to the large bowel. This may lead to inflammation, ulceration and haemorrhage
transient, less severe symptoms, bloody diarrhoea + abdo pain.
‘thumbprinting’ on AXR
conservative management (surgery if peritonitis, perf or ongoing haemorrhage)

nb can also get chronic mesenteric ishaemia - think of like intestinal angina - but this is rare

Question 56

Q

RECTAL BLEEDING

add-on examination to always do? 1
bedside test to do? 1
bloods to do? 8
imaging to consider? 2

Answer

A

always do a DRE (looking for peri anal disease and also visualising blood)

send off stool sample for MC+S

FBC
U+E
LFT
amylase
CRP
clotting
VBG
group + save (cross-match if still actively bleeding)

to CONSIDER:

abdo X-ray
erect CXR (if peritonism or cardio/resp comorbidity)

nb can consider colonoscopy but not while actively bleeding!!

nb keep niol by mouth

nb consider IV omeprazole (as may be an upper GI bleed)

if signs of sepsis or perforation, give Abx

Question 57

Q

What are the five main groups of causes of abdominal distension? 5

(incl way to remember)

Answer

A

“the 5 Fs”

Fluid
Flatus
Faeces
Fat
Foetus

Question 58

Q

Give examples of causes of abdo distension that come under ‘fluid’? 3

what test to do to see if there is fluid on the abdomen? 1

Answer

A

ascites
bladder (retention)
large AAA

SHIFTING DULLNESS

Question 59

Q

If abdominal distension present:

what should you always ask a woman? 1
imaging to consider? 2
other test to consider if suspect ascites? 1

Answer

A

always ask a woman the date of the first day of her last period!!
(ie to see if possibility of pregnancy)

consider:

AXR
abdo USS

ascitic tap if looks like ascites

Question 60

Q

JAUNDICE:

- three groups of causes? which are conjugated and which unconjugated hyperbilirubinaemia?

Answer

A

1) PRE-HEPATIC
- unconjugated

2) INTRA-HEPATIC
- mainly conjugated (may be some unconjugated)

3) POST-HEPATIC
- conjugated

Question 61

Q

Most common aetiology of PRE-hepatic jaundice? (list some examples)

Answer

A

over-production or increased breakdown of RBCs

eg

DIC
malaria

nb can also be due to impaired hepatic intake
- eg some drugs (rifampicin, contrast agents) or right heart failure

nb also can be dt impaired conjugation (eg Gilbert’s syndrome)

Question 62

Q

Causes of INTRA-hepatic jaundice? (5 common, 7 rarer)

Answer

A

basically anything that causes damage to hepatocytes (also often an element of cholestasis too)

= alcohol
= cirrhosis

= liver cancer or mets

= viral hepatitis (A, B, C etc)

CMV
EBV

= certain medications

liver abscess
haemochromotosis
A1-anti-trypsin deficiency
wilson’s
right heart failure

Question 63

Q

Causes of POST-hepatic jaundice? (aka cholestasis)

autoimmune? 2
bile duct obstruction? (2 copmmon, 4 rarer)
iatrogenic causes to consider? 1

Answer

A

primary billiary cirrhosis
primary sclerosing cholangitis

= common bile duct stones / ascending cholangitis

= pancreatic cancer
- cholangiocarcinoma

external compression of bile duct (eg portahepatic lymph node enlargement)
choledochal cyst
biliary atresia

consider MEDICATIONS (fluclox, co-amoxiclav, nitro, sulphonylureas, steroids, prochlorperazine etc)

nb don’t learn meds - just be aware to review meds in someone with jaundice, incl recent abx

Question 64

Q

What other associated symptoms should you ask about if a patient is presenting with jaundice:

local GI? 5
systemic? 7

Answer

A

LOCAL

vomiting (any blood)
abdo pain
abdo distension (ascites)
dark urine
pale stools (or blood)

SYSTEMIC

appetite
weight loss
fatigue
sleep
fevers
itch!!!!
night sweats

(also pitting oedema on legs)

Answer 64

A

MURPHY’S SIGN

push up on liver edge as patient breathes out and then ask them to take a big breath in and if that causes them a lot of pain / to catch breath then murphy’s positive

murphy’s is negative in biliary colic (may be positive or negative in cholangitis)

Answer 65

A

= gastroenteritis

gastric stasis / gastroparesis
= peptic ulcer disease

= intestinal obstruction
- paralytic ileus

= acute cholecystitis
= acute pancreatitis

(nb can also get haematemesis with things like variceal bleeds)

Answer 66

A

ALCOHOL / DRUGS

= alcohol

= antibiotics
= opiates

cytotoxics
digoxin

CNS CAUSES

= meningitis / encephalitis

= raised intracranial pressure
- brainstem lesions

= migraine

motion sickness
labarynthitis / meniere’s

METABOLIC / ENDOCRINE

= uraemia
= hypercalcaemia
= hyponatraemia

= pregnancy
= diabetic ketoacidosis
- addision’s disease

PSYCH

= self-induced
= psychogenic
= bulimia nervosa

OTHERS

= myocardial infarction

= sepsis (UTI, menigitis)
= acute pain (eg ovarian torsion)

autonomic neuropathy

Answer 67

A

what vomit LOOKS like!

what ate?
billious? (green)
frank blood?
coffee ground?
feculent? (small bowel obstruction)

ask about possibility of pregnancy!!!

Answer 68

A

MORNING

prganacy
raised ICP

ONE HR POST FOOD
- gastric stasis / gastroparesis (DM)

PAIN RELIEVED BY VOMITING

peptic ulcer
biliary colic

PRECEEDED BY LOUD GURGLING
- obstruction (esp if also distended)

Answer 69

A

abdo pain
abdo distension
when last opened bowels?
passed FLATUS?
passing urine?

AW FS FIN for systemic

assess for signs of DEHYDRATION hydration status

Answer 70

A

BLOODS:

FBC
U+Es
LFTs
amylase
glucose
VBG
calcium (/bone profile)

(do trop + ECG if suspect MI)

suspect obstruction = AXR

suspect raised ICP = CT head

urine PT on all young women w vomiting

consider endoscopy if persistent vomiting

Answer 71

A

hypokalaemia

if severe, can get a hypochloraemic alkalosis

can see ketones on urine dip if segvere and really not keeping anything down (esp in pregnancy)

Answer 72

A

HISTAMINE (H1)
= cyclizine
- cinnarizine
(safe in preg, vestibular causes)

DOPAMINE (D2) 
= metoclopramide
= domperidone
= prochlorperazine
- haloperidol

SEROTONIN (5HT3)
= ondansetron
(chemical cuases, eg chemo, but 1st line for most things)

OTHERS
= dexamethasone (adjuvant, unknown action, also for raised ICP)
= hyoscine hydrobromide (antimuscarinic)
= midazolam (anti-emetic effect outlasts sedative effect)

Answer 73

A

avoid cyclizine in ELDERLY (and anyone else at risk of delirium)

avoid metoclopramide in:

GI obstruction (as prokinetic)
parkinsons (as can induce EPSE’s)

nb generally avoid metoclopramide as can produce EPSEs in even young otherwise fit people

Answer 74

A

NEUROPATHY
- loss of sensation
- Warm, dry skin, foot pulses are palpable
= 10g monofilament test

PERIPHERAL ARTERY DISEASE
- diabetes is big risk factor for this
- Cool, pale foot with no palpable pulses
= palpate for dorsalis pedis + posterial tibial artery pulse (+/- ABPI)

need regular follow up at diabetic foot clinic:
• deformity or
• neuropathy or
• non-critical limb ischaemia
• previous ulceration or
• previous amputation or
• on renal replacement therapy or
• neuropathy and non-critical limb ischaemia together or
• neuropathy in combination with callus and/or deformity or
• non-critical limb ischaemia in combination with callus and/or deformity
BASICALLY ANYONE WITH ANYTHING MORE THAN A SIMPLE CALLUS!

Nb although diabetic foot is often described as ischaemic or neuropathic - if often an element of both

Answer 75

A

Venous ulcers
= shallow ulcers with a granulated base, often with other clinical features of venous insufficiency present

Neuropathic ulcers
= PAINLESS ulcers over areas of abnormal pressure (eg head of metatarsal bones or heal), often secondary to joint deformity in diabetics ALMOST ALWAYS on SOLE of feet!

Arterial ulcers
= found at distal sites, often with well-defined borders and other evidence of arterial insufficiency

Answer 76

A

aka CHARCOT’S FOOT

The exact cause is unknown. Decreased pain and pressure perception, abnormal strain and weight distribution, as well as autonomic neuropathy that increases perfusion with a subsequent “washing out” of bone substance is suspected.

Tarsus and tarsometatarsal joints most commonly affected
Coexisting ulcers common
Acute: swelling, warmth, erythema
Chronic: painless bony deformities, midfoot collapse, osteolysis, risk of fractures
specialist review for consideration of off-loading abnormal weight
sometimes immobilisation of the affected joint in plaster

Answer 77

A

good glycaemic control prevents!
- also regular screening and self-inspection of feet

do x-ray to look for osteomyelitis / bone deformity - MRI if high clinical suspisiopn

NEUROPATHIC ULCERS

regular chiropody
surgical debridement if appropriate
abx if become infected
may need offloading to allow to heal!
also dressing!
last line = amputation!

if peripheral vascular disease - refer to vascular

Answer 78

A

66% of hyperthyroidism

toxic multinodular goitre
toxic adenoma
too much levothyroxine
(nb can rarely get toxic thyroid tumours and also ovarian/testicular cancers which produce thyroid hormones)

also thyroiditis - eg caused by drugs, radiation etc can rarely cause hyperthyroidism - but norm cause hypo!

GRAVES
- circulating IgG auto-Ab bind to and activate G-protein thyrotropin receptors → smooth thyroid hyperplasia → ↑T3 production

= women aged 30-50
= a/w autoimmune conditions (eg vitiligo, type 1DM, Addison’s)

common triggers:

infection
child birth
stress

Answer 79

A

subclinical = T3/4 are normal but TSH is abnormal!
- Does NOT refer to presence or abscence of symptoms!

subclinical hyperthyroidism:

norm T3/4
low TSH

subclinical hypothyroidism

norm T3/4
high TSH

may or may not be symptomatic!

if symptomatic treat the same as norm! (discuss w pt)
if asymptomatic: norm just observe and repeat in few months!

Answer 80

A

TSH receptor antibodies (TRAb)
= GRAVES (90%)
- may also be raised in hashimotos or multinodular goitre

Thyroid peroxidase antibodies (TPOAb or anti-TPO) 
= HASHIMOTOS (90%)
= POSTPARTUM THYROIDITIS (>60%)
- graves (70%) 
- can rarely be raised in thyroid cancer

Thyroglobulin antibodies (TgAb)
= HASHIMOTOS (80%)
- thyroid cancer (25%)
- other autoimmune diseases (40%)
^not great marker for diagnosis but important for thyroid cancer follow up / monitoring

Answer 81

A

Diffuse, smooth, non-tender goiter

1) THYROID EYE DISEASE (30%)
- Exophthalmos
- Opthalmoplegia (paralysis of muscles within or surrounding eye → diplopia)
- lid lag
- lid retraction
- hjigh risk for corneal ulcers + abrasions

2) PRETIBIAL MYXOEDEMA
- oedematous, discoloured swelling above lateral malleoli (see photos**)

3) THYROID ACROPACHY
- extreme manifestation with clubbing, painful finger + toe swelling,
- periosteal reaction in limb bones

4) THYROID BRUITS
- due to ↑vascularity in thyroid gland

nb not going to describe other symptoms / signs of hyperthyroidism as I’ve done them to death!!
- but remember get OLIGOMENORRHOEA in HYPER (menorrhagia in hypo!)

nb get hypertension with widened pulse pressure:

Systolic pressure is increased due to increased heart rate and cardiac output
Diastolic pressure is decreased due to decreased peripheral vascular resistance

Answer 82

A

see investigation algorithm

1st bloods:

TSH
free T3/4

do thyroid antibody bloods 2nd (after know that hyperthyroid)

TSH receptor antibodies (TRAb)
Thyroid peroxidase antibodies (TPOAb or anti-TPO)
Thyroglobulin antibodies (TgAb)

if cause of hyperthyroid unclear after antibodies endocrinologist can do:

thyroid ultrasound with doppler
radioactive iodine uptake scan

nb if TFTs show secondary hyperthyroidism - refer to endocrinologist for further tests

nb TFTs often normal in thyroid cancer!

nb don’t do radioactive iodine scan if woman is pregnant!

Answer 83

A

control symptoms: BETABLOCKERS - propranolol (until can start Carbimazole - can only be started by an encrinologist!)

nb if someone is unwell at diagnosis - admit them!

1ST line: CARBIMAZOLE

^Can give Carbimazole + Levothyroxine simultaneously (block and replace) – reduces risk of iatrogenic hypothyroidism

nb carbimazole is norm given for 6 weeks until euthyroid then keep at level and gradually reduce - most people are of drugs after 2 years!

if pregnant: PROPYLTHIOURACIL

IF RELAPSE
- Radioactive iodine 
OR
- thyroidectomy
^will need levothyroxine for life after both of these!

nb can’t give radioactive iodine if:

breastfeeding
pregnant (or will becom ein next 6 months!)

Answer 84

A

agranulocytosis
teratogen (make sure on contraception)
cholestatic jaundice (? is this one right? **)

Answer 85

A

nb only get thyroid eye disease in graves - not in any other cause of hyperthyroidism

nb the patient may be eu-, hypo- or hyperthyroid at the time of presentation

SMOKING = biggest risk factor!

Eye discomfort
↑tears
photophobia
ophthalmoplegia + diplopia
↓acuity
afferent pupillary defect (optic N compression)
Exophthalmos
proptosis
conjunctival oedema
corneal ulcers

REFER ASAP!!!

artificial tears
high dose steroids (may need IV)
surgical decompression

^also stop smoking!

Answer 86

A

typically seen in patients with established thyrotoxicosis and is rarely seen as the presenting feature
Iatrogenic levothyroxine excess does not usually result in thyroid storm

TRIGGERS

thyroid or non-thyroidal surgery
trauma
infection (or intercurrent illness)
acute iodine load e.g. CT contrast media
stopping anti-thyroid meds suddenly

^basically anything that causes a big stress/adrenaline response!

confusion + agitation
nausea + vomiting
heart failure
abnormal liver function test (jaundice may be seen clinically)
HTN (with wide pulse pressure)
tachycardia (norm w AF)
FEVER >38.5 deg

^also very sweaty!!

Answer 87

A

nb if lead to congestive heart failure, esmolol is the preferred beta blocker

1) PARACETAMOL
- bring temp down

2) IV PROPANOLOL
- reduce HR
- can use calcium channel blocker if B blocker CI

3) PROPYLTHIOURACIL
- anti-thyroid drug norm used in preg
- better than carbimazole in acute setting

4) POTASSIUM IODINE
- not sure how this works but they give it
- aka Lugol’s iodine

5) DEXAMETHASONE
- blocks the conversion of T4 to T3

ALSO treat UNDERLYING TRIGGER!

call ICU if need help!

Answer 88

A

METFORMIN

reduce glucose absorption (gut)
reduce glucose production (liver)
increase insulin secretion (pancreas)
increase peripheral glucose uptake (fat + muscle)

weight LOSS

CONTRAINDICATIONS

AKI
eGFR < 30

ADVERSE EFFECTS

GI symptoms
lactic acidosis

Answer 89

A

SULFONYLUREAS
- eg gliclazIDE
= stimulates Beta cells in pancreas
- weight GAIN

GLITAZONES
- eg pioGLITAZONE
= reduces peripheral insulin resistance
- weight GAIN

GLIPTINS
- eg sitaGLIPTIN
= stop breakdown of the molecules that stimulate insulin secretion post-food (so insulin stays around longer)
- weight NEUTRAL

GLP-1 MIMICS
- eg exenaTIDE
= Increase insulin secretion, reduce glucagon secretion
- weight LOSS
= this is a SUB CUT injection!

SGLT-2 INHIBITORS
- eg dapaGLIFLOZIN
= Stop glucose being reabsorbed in kidneys (pee out sugar)
- weight LOSS

Answer 90

A

SULFONYLUREAS
- eg gliclazIDE

CI:

Severe renal impair (accumulation can -> hypo)
Porphyria
G6PD deficiency

ADVERSE EFFECTS

Weight gain
Hypos

GLITAZONES
- eg pioGLITAZONE

CI:

Bladder Ca (or high risk)
Liver impairment
Heart failure
Severe renal impairment

ADVERSE EFFECTS

Weight gain
Bladder cancer
Fluid retension

GLIPTINS
- eg sitaGLIPTIN

CI:

Severe liver probs
Hx of pancreatitis
Lower dose in renal impairment - NOT CI!

ADVERSE EFFECTS:

GI symptoms
headaches (BIG PROBS!)
Pancreatitis
Skin probs

GLP-1 MIMICS
- eg exenaTIDE (SC inject)

CI:

eGFR < 30
Hx of pancreatitis
Quite a few tbf

ADVERSE EFFECTS

GI symp
Pancreatitis

SGLT-2 INHIBITORS
- eg dapaGLIFLOZIN

CI:

eGFR <60
Pts at risk of hypotension (eg frail elderly)
Stop during illness if dehydrated

ADVERSE EFFECTS

euglycaemic DKA (+ hhs)
UTIs + thrush
polyuria
Skin rash

Answer 91

A

↓MINERALOCORTICOIDS (aldosterone) from z. glomerulosa → ↓stimulation of Na/K+ pump in kidney → ↑K+↓Na+; ↓water and ↓HCO3- (acidosis) reabsorption into blood

↓GLUCOCORTICOIDS (cortisol) from z. fasciculata →↓gluconeogenesis (formation of glucose from AA) → ↓blood glucose

nb also slight: ↓Androgens → ↓testosterone (mild, most produced in testes)

Answer 92

A

Increases BP by retaining salt (and thus excreting K+)

Answer 93

A

ADDISONS

BP: LOW
Glucose: LOW
Na: LOW
K+: HIGH

CUSHINGS

BP: HIGH
Glucose: HIGH
Na: HIGH
K+: LOW

CONNS:

BP: HIGH
Glucose: norm
Na: HIGH
K+: LOW

Cushings looks like conns because, at high levels, corticosteroids start acting on mineralocorticoid receptors!

Answer 94

A

ADDISON'S (80%)
- autoimmune destruction of adrenal glands
= 30-50y
= females
= PMHx autoimmune conditions

other primary

TB
mets (eg bronchial Ca)
meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
HIV
antiphospholipid syndrome

nb can also get through other causes of haemorrhage / infarction to adrenal glands (incl DIC)

secondary causes:

pituitary disorders (e.g. tumours, irradiation, infiltration)
long-term steroid therapy

Answer 95

A

Lean + Tired:

Anorexia, Weight loss
Dizzy, Syncope, Postural hypoTN

Tanned:
- Bronze skin and pigmented palmar crease + buccal mucosa

Tearful + Weak:
- fatigue, depression, ↓self-esteem, psychosis

GI:
- Nausea, vomiting, abdo pain, diarrhoea or constipation (crave salty food!)

in women can get
↓Androgen symptoms (rarely affects men due to testis)
- ↓Sex drive
- ↓Pubic hair (women)

Primary Addison’s is associated with HYPERPIGMENTATION whereas secondary adrenal insufficiency is not

Answer 96

A

1) 9am CORTISOL

Also:

ACTH (high in addisons)
Adrenal Auto-Ab (+ ve 80% in Addisons)
U+Es (↑K+ ↓Na+ ↓HCO3-, mild ↑Ca2+)
glucose (low)

DIAGNOSTIC TEST: Synacthen® ACTH stimulation test
- repeated blood tests (do in hosp)

AXR/CXR

exclude secondary causes
Identify past TB e.g. upper zone fibrosis or adrenal calcification
Check for lung neoplasms

Answer 97

A

nb usually managed by an endocrinologist

1) GLUCOCORTICOID REPLACEMENT 
= norm hydrocortisone
- give blue steroid card
- tell not to stop abruptly
- DOUBLE dose in acute illness (give IM hydrocortisone pack to use if vomiting prevents oral meds)

2) HYDROCORTISONE REPLACEMENT
= fludrocortisone
(don’t need to double in illness)

nb can also give Androgen replacement: DHEA (Dehydroepiandrosterone)

Answer 98

A

norm cause:
Stress (e.g., infection, trauma, surgery) in a patient with underlying adrenal insufficiency

1) Pain in back, abdomen or legs (can resemble peritonitis)
2) Diarrhoea + Vomiting → Dehydration
3) ↓BP → Hypovolaemic shock →↓Consciousness → Death

(also often have fever)

3 Ss of Mx

1) SALT
- 0.9% saline (a lot!)

2) SUGAR
- 50% dextrose if hypo

3) STEROIDS
- IV hydrosortisone high doses

nb as well as someone with addisons getting this dt acute illness / surgery, can also get with:

adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
steroid withdrawal

Answer 99

A

HASHIMOTOS THYROIDITIS = most common in UK
- may have initial hyper phase

Sub-acute de Quervain’s thyroiditis
= thyroiditis following viral infection → hyperthyroidism (phase 1) → euthyroid → hypothyroid (phase 3) = painful goitre
- self-limiting

Riedel’s thyroiditis
= fibrous replacement of thyroid parenchyma → painless goitre

Post-partum thyroiditis
= initial hyper phase -> prolonged hypothyroid phase

Iodine deficiency
= most common cause worldwide

drug-induced

LITHIUM
anti-thyroid drugs (eg carbimazole)
AMIODARONE (can cause hyperthyroid)

post-hyperthyroid Mx
- following radioiodine ablation or thyroidectomy

Congenital

can be sporadic or inherited
very serious if not picked up!

secondary hypothyroid is rare!! - norm from pituatory failure

nb
Non-painful Goitre – Hashimoto and Riedel
Painful Goitre – De-Quevain

Answer 100

A

Female (5-10 times more common)

type 1 DM
addison’s
perncious anaemia
Down’s syndrome
Turner’s syndrome
coeliac disease

Answer 101

A

Weight gain despite loss of appetite
Fatigue, Lethargy ↑Sleeping,↓Mood
↓Memory + ↓Cognition → dementia like symptoms
Constipation
MENORRHAGIA
Hoarse voice
Cold Sensitivity
Myalgia + Cramps
↓Libido
Dry skin + Hair loss/thinning + Cold Hands
(± loss of lateral eye brows)
↓HR (bradycardia) ↑BMI
↓Reflexes
Oedema (swelling in skin + soft tissue, typically lids, hands, face, tongue)
Peaches + cream complexion + Round puffy face

may get Ascites, Pericardial or pleural effusion

may also get cerebellar ataxia

Answer 102

A

TSH (high in primary, low in secondary)
T3/4 (low in both)
autoantibodies (anti-TPO) - positive in hashimotos

?refer all to endocrinologist

TSH used for monitoring primary! (if secandary need T3/4 too)

LEVOTHYROXINE (T4)
- review every 3-4wks until stable TSH - then r/v 4-6 months

^if elderly or IHD then start very low dose and slowly build up!

SIDE EFFECTS:

hyperthyroidism (over treatment)
worsen angina
worsen AF
osteoporosis

nb if high TSH and norm T3/4 then norm means non-compliance with levothyroxine

nb Iron reduces absorption of levothyroxine – give at least 2hrs apart

Answer 103

A

poorly controlled hypothyroidism who undergo infection or surgery

low GCS (or confusion)
hypothermia

Mx

IV thyroid replacement
IV fluid (incl IV electorylte correction)
IV corticosteroids (until the possibility of coexisting adrenal insufficiency has been excluded)
sometimes rewarming

Answer 104

A

aka non-thyroidal illness syndrome

no thyroid symptoms
- just abnormality in TFTs when someone is acutely unwell (esp in ICU)

NORM LOW T3
- T4 nd TSH are normal or low

Changes are reversible upon recovery from the systemic illness and hence no treatment is usually needed

Answer 105

A

PTH

pulls calcium from bone
decreased calcium loss in urine, loose more phosphate (and activate vit D)
increased absorption of calcium from gut

PRIMARY
= Increased PTH secretion from PTH gland
= norm dt single parathyroid ADENOMA
- High PTH (or can be norm!), high Ca2+
- low phsophate, rasied ALP

SECONDARY
= Hypocalcaemia (norm dt CKD) -> reactive (and appropriate) increase in PTH
- High PTH, low (or norm) Ca2+
- high phosphate
- low Vit D

TERTIARY 
= prolonged secondary → hypertrophy of PTH gland -> release PTH independent of Ca2+ levels 
- Very high PTH, high Ca2+
- low or norm vit D
- low or norm phosphate
- high ALP

nb phosphate norm does opposite to calcium

so hypercalcaemic crisis may occur in primary or tertiary (but not secondary!

Answer 106

A

PRIMARY
= PTH gland adenoma (85%)
- hyperplasia / multiple adenomas (15%)
- carcinomas (0.5%)
- MEN (multiple endocrine neoplasia) type 1 or 2

SECONDARY
= CKD
- malnutrition
- vit D deficiency (low sun, nutritional deficiency, liver cirrhosis)
- cholestasis (need bile to absorb fat-soluable vits like vit D)

nb parathyroid adenoma most common in post-menopausal/elderly women!

Answer 107

A

the MAJORITY of pts with primary hyperparathyroidism are ASYMPTOMATIC!

STONES
- renal colic

BONES

bone, muscle + joint pain
fragility fractures
pseudogout
Osteitis fibrosa cystica (cyst-like brown tumors)
Skull: granular decalcification (salt-and-pepper skull)

ABDO GROANS
- anorexia
- nausea (+ vomiting)
- constipation
= gastric or duodenal ulcers (get dyspepsia 1st)
- pancreatitis

THRONES
= polydipsia + polyuria + dehydration (nephrogenic diabetes insipidus)

PSYCH OVERTONES

Depression
confusion
hallucinations
coma

OTHER

hyporeflexia
muscle weakness
malaise

short QT interval (rarely seen)

can also get HYPERTENSION

if severe can also get: Osteitis fibrosa cystica (severe) – pts. w/ sub-periosteal resorption of distal phalanges, tapering of distal clavicle, salt and pepper skull, brown tumours of long bones

Answer 108

A

BP will often be raised!

Calcium = high
PTH = high (or norm!!)
phosphate = low
ALP = high

can also do a DEXA scan to determine levels of osteoporosis/dystrophy

to lower Ca = LOTS of saline!!! (forces diuresis - may need to replace K and Mg as these will also lower, as well ac Calcium)

AVOID THIAZIDE diuretics! (will raise calcium further!)

(if really bad can have dialysis / haemofiltration)

definitive = TOTAL PARATHYROIDECTOMY (surgery)

if unfit for surgery: CINACALCET (calcimimetic) → ↑sensitivity of parathyroid cells to ca2+ levels → ↓PTH secretion
- may also use bisphosphonates if have osteoporosis

nb conservative management may be offered if the calcium level is less than 0.25 mmol/L above the upper limit of normal AND the patient is > 50 years AND there is no evidence of end-organ damage AND asymptomatic!

Answer 109

A

Malignancy

parathyroid related protein is produced by SCC lung cancer (breast and renal too) → mimics PTH → high calcium!

Answer 110

A

TREAT UNDERLYING CONDITION (ie norm CKD)

phosphate dietary restriction +/- phosphate binders
activated vit D (if deficienct)

Answer 111

A

Allow 12 months to elapse following kidney transplant as many cases will resolve with this

The presence of an autonomously functioning parathyroid gland may require surgery. If the culprit gland can be identified then it should be excised. Otherwise total parathyroidectomy and re-implantation of part of the gland may be required.

Answer 112

A

nb hyperklipidaemia and dyslipidaemia are used interchangably!

predominantly high TRIGLYCAERIDES

obesity
alcohol
diabetes (type 1 + 2)
CKD
liver disease

MEDS high TRIGLYCERIDES

thiazide diuretics
non-selective beta blockers
unopposed oestrogen

predominantly high CHOLESTEROL

nephrotic syndrome
cholestasis
hypothyroidism

can get various different hereditary hyperlipidaemia and hypercholesteraemias
- often present at a young age and don’t necessarily have obesity etc

nb other drugs that cause dyslipidaemia are antipsychotics, corticosteroids or immunosuppressant drugs

Answer 113

A

most diagnosed on routine screening (ie asymptomatic!)

nb Xanthoma = nodular lipid deposits in the skin and tendons

TENDINOUS XANTHOMAS: firm nodules, located in tendons (typically extensor tendons of hands and the Achilles tendon)

PALMAR XANTHOMAS: yellow plaques on the palms of the hands

XANTHELASMAS: nodular lipid deposits around the eyelids
- nb can be seen without lipid abnormalities!

PREMATURE CORNEAL ARCUS:
white grey opaque ring in corneal margin

nb can also have eruptive xanthomas in familial causes on extensor surfaces (are red and yellow)

Answer 114

A

bloods = FULL LIPID PROFILE
- Tchol, HDL-C, non-HDL-C, TG concentrations

nb can do other bloods to rule out secondary causes: eg U+Es, TFTs, LFTs

BMI (norm BP too)
QRISK 2
dietary advice
increase exercise
stop smoking

statin if high QRISK 2 (see other flashcard)

Answer 115

A

anyone over the age of 40 (check this age with NICE CKS!!***)

if >10% QRISK then start 20mg atorvastatin ON

give 20mg atorvastatin (regardless of QRISK2)

CKD eGFR<60
all adult type 1 diabetes
familial hyperlipidaemia (may be higher dose!)

give 80mg atorvastatin for secondary prevention

any IHD
ischaemic stroke
peripheral artery disease

Answer 116

A

decrease PTH norm secondary to thyroid surgery (nb this is still called primary though…)
autoimmune
di-george syndrome

PSEUDOHYPOPARATHYROIDISM
= abn G protein → failure of target cell response to PTH
- Sx = short stature, low IQ, short 4th/5th metacarpals, round face
- bloods: ↓Ca2+ ↑PO4- ↑PTH

PSEUDOPSEUDOHYPOPARATHYROIDISM
= morphological features of above but normal biochem

Answer 117

A

dt HYPOCALCAEMIA

Tetany – muscle twitch, cramping, spasm

Bone pain – turnover abnormally low → ↑mineral density

Perioral paraesthesia

TROUSSEAU’S SIGN
- carpal spasm if brachial artery occluded by inflating BP cuff

CHVOSTEK’S SIGN
- tapping over parotid stimulates facial nerve → facial muscle to twitch (detects latent tetany)

Answer 118

A

low calcium = prolonged QT interval

high calcium = shortened QT interval

Answer 119

A

PRIMARY hypoPTH

↓Ca
↑Phos
↓PTH
normal ALP

PSEUDO hypoPTH - ↓Ca

↑Phos
↑ or normal PTH

can do U+Es to exclude CKD and Vit D to exclude deficiency
^can also cause low calcium (secondary hyperparathyroidism!)

PSEUDO hypoPTH

Urinary cAMP
phos post-PTH infusion

Mx = ALFACALCIDOL (active vit D - doesn’t need kidneys to activate!) ? plus calcium supplements?

Answer 120

A

PAPILLARY (70%)
- typically young pts
- hist: papillary projections + pale empty nuclei
= total thyroidectomy (+/- node excision +/- radioiodine)
= yearly thyroglobulin levels to detect early recurrent disease

FOLLICULAR (20%)
- typically middle aged
- hist: encapsulated with capsular invasion
= total thyroidectomy (+/- node excision +/- radioiodine)
= yearly thyroglobulin levels to detect early recurrent disease

MEDULLARY (5%)
- MEN syndrome (although 80% are sporadic!)
- may produce calcitonin (opposite to PTH)
= total thyroidectomy
= phaecromocytoma screen

ANAPLASTIC

elderly females
can comonly cause local pressure symptoms
poor prognosis: not responsive to Mx

LYMPHOMA (rare)
- females with hashimotos

Answer 121

A

tumours do NOT commonly secrete thyroid hormones so features of hyper/hypothyroidism are RARE

75% are asymptomatic!!!
- firm painless thyroid nodules may be present!

possible late features:

Dyspnoea
Dysphagia
Hoarseness (vocal cord paresis)
Horner syndrome
Possible SVC obstruction

USS thyroid = 1st investigation!

Answer 122

A

nb with thyroid: toxic = functioning (ie changes TFTs)

symptoms of HYPERthyroidism (+ nodular goitre) - do TFTs and see primary HYPERthyroid
- is 2nd most common cause (25%) after graves

RISK FACTORS

elderly
iodine deficient

10% of multinodular goitres (ie not-toxic) -> toxic multinodular goitres

Nuclear scintigraphy shows PATCHY UPTAKE

Mx

if just hyperthyroid -> radioiodine treatment
if also causes local symptoms (dysphagia/dyspnoea etc) -> surgery

nb don’t norm use carbimazole in toxic multi-nodular goitre!

can use betablockers to control symptoms before referral!

Answer 123

A

symptoms of HYPERthyroidism (+/- palpable nodule) - do TFTs and see primary HYPERthyroid
- is 3rd most common cause (5-10%)

female > male
30-50 years

Thyroid scintigraphy:
= solitary, hot nodule

(Shows radioiodine uptake by the hyperfunctioning nodules with suppression of rest of the gland)

unsure on mx (but don’t need to know as brief CC)

nb is benign!

Answer 124

A

DIFFUSE (HYPER)

Graves
TSH-secreting pituitary adenoma (rare)

DIFFUSE (HYPO)
- hashimoto's
- sub-acute de quervain's (hyper first) (is PAINFUL)
- riedel's 
?postpartum too

DIFFUSE (EU)
- iodine deficiency (can eventually lead to hypo OR hyperthyroid)

NODULAR (HYPER)

toxic multi-nodular
toxic adenoma / nodule

NODULAR (EU)
- thyroid cancer
- non-toxic adenoma
- cysts
(also other causes of neck lumps)

do TFTs and USS thyroid

Answer 125

A

Compression of the TRACHEA
→ exertional dyspnea and, in severe cases, stridor or wheezing

Compression of the OESOPHAGUS
→ dysphagia

nb not sure if hoarse voice is due to hypothyroidism or due to compression from goitre!

Answer 126

A

May only have supression of some of these hormones!!! - ie not all! - if all = panhypopituitarism

GROWTH HORMONE deficiency (see other flashcard)

PROLACTIN deficiency → lactation failure following delivery (how Sheehan’s often picked up!)

FSH/LH deficiency → hypogonadotropic hypogonadism (secondary hypogonadism)

TSH deficiency → secondary hypothyroidism

ACTH deficiency → secondary adrenal insufficiency (do NOT get tanned skin, unlike in addisons)

^these are all ANTERIOR pituatory hormone

if hypopit is extensive / caused by compressive aetiology then can get deficiency of POSTERIOR pituatory hormones:

ADH deficiency → central (neurogenic) diabetes insipidus
Oxytocin deficiency → no effect

nb if hypopit is caused by a space occupying lesion then will also get neuro/ opthalmic symptoms (see later flashcards on pituatory adenomas)

Answer 127

A

IN CHILDREN

growth retardation (during childhood)
↓ bone density
muscle atrophy
hypercholesterolemia

IN ADULTS (is subtle!)

Central obesity
Dry, wrinkly skin
↓Strength ↓Balance ↓Exercise ability
depression

tbh basically the same but obvs doesn’t affect growth in adults!

Answer 128

A

WOMEN

Oligomennorhoea or Amenorrhoea
↓Fertility, ↓Libido, Dyspareunia
Breast atrophy

MEN

Erectile dysfunction
↓muscle bulk
Hypogonadism (↓hair, small testes, ↓ejaculate vol, ↓sperm)

Answer 129

A

sequence:
1) GH and prolactin
2) → FSH → LH
3) → TSH
4) → ACTH

Because hypoprolactinemia is typically asymptomatic (except failure to lactate following delivery),

GROWTH RETARDATION is the first presenting symptom among CHILDREN and

HYPOGONADISM is the first clinical feature among ADULTS

Answer 130

A

COMPRESSIVE CAUSES
= non-secretory pituatory macroadenoma (most common - 40% in adults!)
- internal carotid aneurysms
- meningiomas
- craniopharyngioma
- Rathke's cleft cyst

OTHER

pituatory apoplexy (infarction of gland - incl Sheehan’s)
traumatic brain injury
iatrogenic (eg surgery to remove adenoma / pituatory irradiation)
infiltaration of pituatory +/or hypothalamus (haemochromatosis, meningitis, TB)

nb pituatory apoplexy presents suddenly: severe headache, sudden hypotension, hypovolemic shock

nb in sheehan’s often have a postpartum haemorrhage but can occur without clinical evidence of haemorrhage

see amboss if want to know full investigations and management etc of hypo pit!

but is basically measuring all the affected hormones and then replacing the ones that are deficient! (and surg/radio removal of anything compressing gland)
nb always replace corticosteroids before thyroid hormones (as levothyroxine can precipitate adrenal crisis if ACTH deficiency!)

Answer 131

A

MACRO = over 1cm
MICRO = under 1cm

secretory or non-secretory!

1) PROLACTINOMA (40%)
- Women: galactorrhea, amenorrhea, reduced bone density due to suppression of estrogen
- Men: reduced libido and infertility

2) NON-SECRETORY (35-40%)
- can cause hypopit by mass effect (copmmonest cause of hypopit - develops slowly!)

3) SOMATROPH (10-15%) (ie GH)
- acromegaly or gigantism!

4) CORTICOTROPH (5%) (ie ACTH)
- cushing’s DISEASE
- aka secondary hypercortisolism

5) THYROTROPH (1%) (ie TSH)
- secondary hyperthyroidism

6) GONADOTROPH ADENOMA (rare) (ie LH, FSH)
- rare! most non-functioning!

nb Most secrete one pituitary hormone, with hyperplasia of only one type of endocrine cell.
- The presence of multiple pituitary hormones should also raise the suspicion of atypical pituitary adenomas or pituitary carcinomas

nb Mild hyperprolactinemia in a patient with a pituitary adenoma does not necessarily imply that the tumor is a prolactinoma; any sellar tumor can disrupt the inhibitory effect of the hypothalamus on the pituitary gland, which can result in hyperprolactinemia

Answer 132

A

1) HORMONE EFFECTS
- hypo-pit if nonsecretory or effects of excess hormones if secretory

2) VISUAL FIELD DEFECTS
- bitemporal hemianopia (dt compression of optic chiasm)
- can less commonly also get squint and double vision dt CN 3, 4 +/or 6 palsy (not sure which most common)

3) HEADACHE
- dt stretching of dura
- worse on coughing, head down etc

nb visual field defects are normlaly reversible with removal of adenoma (though not always)

Answer 133

A

INVESTIGATIONS

1) pitutatory blood profile (incl GH, prolactin, ACTH, FH, LSH and TFTs)
2) formal visual field testing
3) MRI brain with contrast

MANAGEMENT

hormonal therapy (e.g. BROMOCRIPTINE is the first line treatment for prolactinomas)
surgery (e.g. transsphenoidal transnasal hypophysectomy) if large / increase in size
radiotherapy

nb non-functioning microadenomas are very common (?10% of pop) but don’t cause any symptoms or problems - BUT if you pick an adenoma up incidentally you need to do hormone panel to work out if functioning or not!

nb Bromocriptine is a dopamine receptor agonist! - has inhibitory effect on prolactin production

Answer 134

A

ie too much GROWTH HORMONE

Coarse facial appearance, wide nose, puffy lips, eyelids
Excessive sweating, oily skin
↑Growth of hands (spade-like), jaw, feet, tongue
Dark skin, acanthosis nigricans
Amenorrhoea, ↓Libido
Sleep apnoea
Proximal weakness and arthropathy

nb if in kids (ie before growth plates fused) then get gigantism

THIS IS NOT EVEN A CORE CONDITION - I just found interesting!

Answer 135

A

too much exogenous CORTICOSTEROID USE / stopping steroids too quickly
- can also get following treatment of cushing’s disease (ie removal of pituatory tumour)

dt prolonged high corticosteroid levels having a negative feedback loop and suppressing hypothalamus and pituatory which then atrophy over time

presents like addisons! - either slowly or suddenly in addisonian crisis!

prevent by:

avoiding long-term steroid use
tapering steroids slowly is used for more than a week!

Answer 136

A

Rare catecholamine tumour arising from adrenal medulla
-> ↑Adrenaline + ↑Dopamine

10% are familial

MEN type II
neurofibromatosis
von Hippel-Lindau syndrome

rule of 10%

bilateral in 10%
extra-adrenal in 10%
malignant in 10%

features are typically EPISODIC

headaches
anxiety
palpitations
sweating
tachycardia
HTN (90% - may be sustained)

nb extra-adrenal norm at organ of Zuckerkandl adjacent to aorta bifurcation

Answer 137

A

24 hr urinary collection of metanephrines

nb used to be 24 hr urinary collection of catecholamines but this is less sensitive

stabilise with:
1) alpha-blocker (e.g. PHEnoxybenzamine)

given before a

2) beta-blocker (e.g. propranolol)

always give ALPHA blocker first (A before B)

definitive mx = SURGERY!

Answer 138

A

ACTH INDEPENDENT
= ie just lots of corticosteroids 
= EXOGENOUS STEROIDS
- benign adrenal adenoma (5%)
- adrenal nodular hyperplasia (rare)
- Mc-Cune-Albright syndrome

ACTH DEPENDENT
= ie somehting’s producing too much ACTH
- cushing’s disease (benign pituatory adenoma) (80%)
- ectopic ACTH (eg from SMALL CELL LUNG CANCER) (5-10%)

Answer 139

A

↑Weight (significant) → Obesity

Muscle weakness + wasting → PROXIMAL MYOPATHY

-ve mood change – depression, LETHARGY, irritability, psychosis

GONADAL DYSFUNCTION (↓GRH) – irregular periods, hirstuism, erectile dysfunction

ACNE

Infection prone + Poor healing wounds (↓inflam mediators)

Risk of RECURRENT ACHILLES TENDON RUPTURE
osteoporosis

plus all the other side effects of steroids…

Answer 140

A

Central/truncal obesity, Moon face, Buffalo neck hump
Skin and muscle atrophy
HTN (↑BP) Hyperglycaemia (↑Glucose)
Bruises + Purple abdominal striae

may see METABOLIC ALKALOSIS (with a low K+)
^ectopic ACTH especially give VERY low K+ levels

Answer 141

A

also obvs you check their meds first - if on steroids then that’s the cause and no more investigations needed!!!

1st
= overnight dexamthasone suppression test
- or 24 hr urinary free cortisol

if cushing’s regardless of cause: cortisol will stay high (will be low if norm)

2nd = 9am and midnight plasma ACTH (and cortisol) levels

if ↓ACTH then ACTH-independent (eg adrenal adenoma)
if ↑ACTH then ACTH-dependent (either pituatory or ectopic ACTH)

^both have high cortisol!

if ACTH-dependent then:

3rd) high dose dexamethasone suppression
- if pituatory = cortisol suppressed
- if ectopic = cortisol stays same!

^ie ectopic ACTH just doesn’t respond to negative feedback etc

nb can also do CRH stimulation test but ?not as good

nb management:

Cushing’s syndrome – give Metyrapone
Iatrogenic = Stop medications i.e. steroids
Cushing’s disease – Removal of pituitary adenoma SE: ↑pigmentation
Adrenal adenoma – Adrenalectomy and adjuvant radiotherapy
Ectopic ACTH – resection of tumour or alternatively Metyrapone, Ketoconazole or Fluconazole → ↓cortisol secretion

Answer 142

A

Pseudo-Cushing’s mimics Cushing’s
- get false positive dexamethasone suppression test or 24 hr urinary free cortisol

causes
- alcohol excess 
- severe depression
- obesity
(also ? rifampicin and phenytoin)

insulin stress test may be used to differentiate

Answer 143

A

bilateral adrenal hyperplasia (BAH) (70%)
unilateral adrenal adenoma (Conn’s)

(rarely can be adrenal carcinoma)

norm no symptoms!!! (may occasionally get features of low K+)

HTN
low K+
high Na
alkalosis

nb in real life only 10-40% have low K+

Answer 144

A

DIAGNOSTIC
= plasma Renin:Aldosterone ratio
- ↑Aldosterone ↓Renin

(if renin is high or normal, it excludes diagnosis of primary hyperAld – likely secondary)

2nd) HIGH-RESOLUTION CT abdomen and adrenal vein sampling is used to differentiate between unilateral and bilateral sources of aldosterone excess

Mx

adrenal adenoma: surgery
bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone

Answer 145

A

high aldosterone due to high renin from ↓renal perfusion

renal artery stenosis
accelerated HTN
diuretics
CHF (hypoperfusion)
hepatic failure

Ix - ↓K+ ↑Na+, ↑Aldosterone ↑Renin

^ie same as primary but HIGH RENIN!

Answer 146

A

very rare to get isolated hypoaldosteronism
- it’s normally the first sign of Addison’s / autoimmune primary adrenal insufficiency (ie before loose corticosteroids)

DON’T get hypoaldosteronism if secondary (ie low ACTH) or tertiary (ie low CRH) adrenal insufficiency!

Answer 147

A

Hirsutism = androgen-dependent hair growth in women
- e.g on the chin, above the upper lip, and around the umbilicus

hypertrichosis = androgen-independent hair growth (eg in anorexia nervosa)

Answer 148

A

Polycystic ovarian syndrome = commonest

Other causes include:

Cushing’s syndrome
congenital adrenal hyperplasia
androgen therapy
obesity (dt insulin resistance)
adrenal tumour
androgen secreting ovarian tumour

drugs:
- phenytoin
- corticosteroids

Answer 149

A

FERRIMAN-GALLWEY scoring system: 9 body areas are assigned a score of 0 - 4, a score > 15 is considered to indicate moderate or severe hirsutism

weight loss (if overweight)
cosmetic techniques (eg waxing/bleaching) - not available on the NHS
consider COCPs
facial hirsutism: topical EFLORNITHINE (CI: pregnancy + breast-feeding)

ALSO TREAT UNDERLYING CAUSE!!!!

Answer 150

A

NEUROGENIC / CRANIAL
= deficiency of ADH secretion 
- idiopathic (50%)
- post head injury
- pituitary surgery
- craniopharyngiomas
- histiocytosis X
- DIDMOAD 
- haemochromatosis

NEPHROGENIC
= insensitivity to ADH
- genetic causes
- electrolytes:↓K+ ↑Calcium 
- drugs: demeclocycline, LITHIUM
- tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis

both types:
impaired water resorption in kidney → ↑excretion of large volumes (>3L/day) of dilute, low urine osmolality (<300 mOsmol/kg) and high serum osmolality > 300

> SYMPTOMS:
polydipsia
polyuria

incl nocturia (adults) or nocturnal enuresis (children)

nb DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)

Answer 151

A

nb have HIGH SODIUM!! (effectively very dehydrated!)

main DDx = diabetes mellitus! (do glucose!!)

1st) serum and urine osmolarity
- serum = high
- urine = low

nb a urine osmolality of >700 mOsm/kg excludes diabetes insipidus

2nd) water deprivation test
= tests ability of kidneys to concentrate urine for diabnosis of DI, and to localise cause
- Deprive fluids 8hrs and test urine osmolality THEN repeat but with 2 mcg desmopressin (synthetic ADH)

NEURO/CRANIAL
= low urine osmolality < 300 before desmopressin, >800 after desmopressin
- Mx: DESMOPRESSIN (also do hormone bloods and MRI pituatory to find cause)

NEPHRO
= low urine osmolality < 300 mosm before AND after desmopressin
- Mx:
— treat cause
— thiazide diuretics (bendroflumethiazide)
— NSAIDs (lower urine vol and plasma Na+)

Answer 152

A

excessive secretion of ADH from the posterior pituitary or an ectopic source → ↑reabsorption of water at collecting duct → hypervolaemia and dilution of electrolytes (↓Na+)

LOW SODIUM (in absence of hypovolaemia, oedema or diuretics)

Urine and plasma osmolarity

urine = high
plasma = low

^ie opposite of diabetes insipidus!

Answer 153

A

MALIGNANCY
= small cell lung cancer
(- pancreas)
(- prostate)

NEURO

stroke
SAH
sub-dural haemorrhage
meningitis/encephalitis/abscess

INFECTION

TB
pneumonia (esp atypical)

MEDS

SSRIs
tricyclics
carbamazepine
vincristine
cyclophosphamides
sulfonylureas

OTHER

positive end-expiratory pressure (PEEP)
porphyrias

Answer 154

A

Fluid restriction
- must be slow due to risk of central pontine myelionlysis (if raise Na too quickly!)

Demeclocycline
- ↓responsiveness of collecting tubule to ADH

nb see hyponatraemia flashcards for more indepth Mx

Answer 155

A

abnormal amount of breast tissue in males, usually caused by an increased oestrogen:androgen ratio

important to differentiate the causes of galactorrhoea (due to the actions of prolactin on breast tissue) from those of gynaecomastia

Answer 156

A

normal in puberty (also for male infants!)

syndromes with androgen deficiency (kallman’s, klinefelter’s)
testicular failure (eg mumps)
liver disease (liver can’t break down oestrogen)
testicular cancer (e.g. seminoma secreting hCG)
ectopic tumour secretion
hyperthyroidism
haemodialysis

Answer 157

A

commonest = SPIRONOLACTONE!

cimetidine (H2 antagonist)
digoxin
finasteride (blocks testosterone activation to shrink prostate)
cannabis
anabolic steroids
GnRH agonists e.g. goserelin, buserelin (puberty blockers)
oestrogens

nb GnRH blockers have lots of uses (also in fibrids, part of IVF, CAH)

nb can also very rarely be caused by other drugs:
tricyclics
isoniazid
calcium channel blockers
heroin
busulfan
methyldopa

Answer 158

A

differentiate this from urinary frequency!! - eg caused by UTI / STI / pregnancy (norm have other symptoms like urgency =?-dysuria or abdo pain)

this is weeing a large amount of VOLUME!!

Diabetes Mellitus (T1 or 2)
Diabetes Insipidous (cranial or nephro)
hypercalcaemia
chronic kidney disease
psychogenic (compulsive water drinking)
DIURETICS (also SGLT-2 inhibitors (eg dapaGLIFLOZIN))

remember LITHIUM is an important cause of NEPHROGENIC diabetes insipidous

1ST LINE = TEST FOR DIABETES MELLITUS (most common cause!)

Answer 159

A

1) SERUM OSMOLARITY

if HIGH (hypertonic hypernatraemia): 
- norm very high glucose (DKA of HHS) which is increasing osmolarity - so fix that then recheck Na!

if NORM (isotonic hyponatraemia):

TURP syndrome
pseudohyponatraemia (ie sodium is actually norm but measures as low dt high amounts of protein or lipids in plasma - eg hyperlipidaemia or multiple myeloma)

if LOW (hypotonic hyponatraemia):
- TRUE hyponatraemia (then do the other investigations - see below, to find cause!)

^this is all in the context of LOW SODIUM!

IF PATIENT IS SYMPTOMATIC +/or SEVERE (eg seizures, coma, resp depression) then just TREAT with hypertonic asaline (+work out cause later!)

2) assess VOLUME STATUS
- hypovolaemic
- euvolaemic
- hypervolaemic
(see other flashcards for causes)

3) URINE OSMOLARITY (+/or sodium)
- high
- low
(compare to serum osmolarity)
(see other flashcards for causes)

Answer 160

A

HYPOvolaemia + HIGH urine Na
= RENAL LOSSES (can't conc urine!)
- diuretic excess (?norm thiazides)
- primary adrenal insufficeincy (addison's)
- cerebral salt wasting syndrome
- renal tubular acidosis
- salt-losing nephropathy

HYPOvolaemia + LOW urine Na
= EXTRARENAL LOSSES (kidney's working but just loosing a lot of fluid + salt)
- vomiting
- diarrhoea
- burns
- pancreatitis
- trauma
- third spacing (don't worry about)

nb see a better flow chart of all of this on my exam notes

Answer 161

A

EUvolaemia + HIGH urine Na

SIADH (very high urine Na!!)
severe hypothyroidism
secondary adrenal insufficiency
diuretics (ie before become hypovalemic)

EUvolaemia + LOW urine Na
= appropriate body reaction!
- primary/psychogenic polydipsia
- beer potomania
- exercise-induced
- tea + toast diet

nb see a better flow chart of all of this on my exam notes

Answer 162

A

HYPERvolaemia + HIGH urine Na
- renal failure (diuretic phase) (again can’t concetrate urine!)

HYPERvolaemia + LOW urine Na

congestive heart failure
liver cirrhosis
nephrotic syndrome

remember these people are opverloaded with fluid!!!

nb see a better flow chart of all of this on my exam notes

Answer 163

A

1) DURATION of hyponatremia: is it acute or chronic?
2) SEVERITY of hyponatremia: what is the sodium level?
3) SYMPTOMS: is the patient symptomatic?

Acute hyponatremia:
- Develops over < 48 hours
- Usually from excessive fluid intake, either parenteral or oral
- Common examples include post-operative parenteral fluids and athletes
= Symptoms are usually severe

Chronic hyponatremia:

If for >48hrs OR duration is unknown
Symptoms are usually less severe than acute
HIGHER CHANCE of causing Osmotic demyelination syndrome (aka central pontine myelinolysis) if correct too quickly!

Answer 164

A

MILD
= 130-134 mmol/l
- none or non-specific symp (headache, lethargy, nausea, vomiting, dizziness, confusion, muscle cramps)
1) fluid restriction
2) LOOP diuretics (if hypervolaemic)

MODERATE
= 120-129 mmol/l
- (same as mild)
1) fluid restriciton
2) LOOP diuretics (if hypervolaemic)
3) 0.9% saline (be careful if already hypervolaemic)

SEVERE
= Less than 120 mmol/l
- Seizures, coma, and respiratory arrest
1) HYPERTONIC SALINE (1.8%) +/- loop diuretics
2) consider CONIVAPTAN (ADH receptor antagonist!)

Can get symptoms at any level! - esp if acute drop! - if severe symptoms! - treat as SEVERE! (regardless of numbers)

nb conivaptan is hepatoxic if have underlying liver disease!

Answer 165

A

ACUTE
- max 1mmol/hr (24mmol/day) (check w senior first!)

CHRONIC
- max 10mmol/day

ie do repeated U+Es to check!!

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3) GI system 2 + endocrinology Flashcards

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