3) GI system 2 + endocrinology Flashcards
ACHALASIA
- what is it? describe the pathology?
= 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
ACHALASIA:
- initial symptoms? 3
- late symptoms / signs? 2
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)
ACHALASIA:
- most serious DDx to consider?
- red flags that may indicate this?
oesophageal or mediastinal cancer
- Weight loss
- loss of appetite
- fatigue
- haematemesis
- Supraclavicular node
→ urgent endoscopy (not barium enema)
ACHALASIA:
- distinctive sign on barium swallow? 1
- gold-standard test? 1
oesophageal dilatation followed by stricture at lower oesophageal sphincter (BIRD BEAK SIGN)
nb aka rat tail sign (I think more accurate)
manometry = gold-standard
GASTRITIS:
- most comon causes? 4
- symptoms? 3
- alcohol
- NSAIDs
- H.pylori
- reflux / hiatus hernia
ALARMS symptoms which are red flags for more serious aetiology than gastritis? 6
Anaemia
Loss of weight
Anorexia
Recent onset or progressive symptoms
Melaena or Haematemesis
Swallowing difficulty (dysphagia)
also new onset over 50!
GASTRITIS:
- test if suspect H.Pylori cause?
- investigation if suspect more serious pathology / redf flags? 1
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
GASTRITIS:
- management if H. Pylori-induced?
- management if not H Pylori induced? 2
H. Pylori = triple therapy
- 2 abx, 1 PPI
If NOT h pylori
- stop nsaids / alcohol
- PPI for 8 weeks
CHRONIC PANCREATITIS:
- what is it?
- most common causes? 2
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
CHRONIC PANCREATITIS:
- main two symptoms?
- symptoms / signs if exocrine mainly affected? 2
- symptoms if endocrine mainly affected/ 3
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.)
CHRONIC PANCREATITIS:
- bloods to do? (and findings)
- findings on USS and CT scans? 1
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!!!
CHRONIC PANCREATITIS:
- diet modification? 2
- mainstay of medical management? 3
- possible indications for surgery? 3
- prognosis?
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
SUBPHRENIC ABSCESS
- what is it?
- what two things is it normally caused by / secondary to? 2
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
SUBPHRENIC ABSCESS
- describe the clinical presentation?
- what is the timescale of the onset of presentation with respect to timeline of cause?
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)
What can be seen on a CXR of a person with a subphrenic abscess?
other imaging done?
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
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)
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
LIVER ABSCESS
- localised symptoms + signs? 2
- systemic symptoms? 5
- 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
PYOGENIC (ie bacterial) LIVER ABSCESS
- most common cause of pyogenic abscesses? (not organism but cause)
- other causes?
- broad principles of management?
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!
AMOEBIC ABSCESS
- norm causative organism?
- what to ask in history in british patients to assess risk?
- broad principles of management?
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!)
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
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)
risk factors for hepatocellular carcinoma:
- lifetyle? 1
- medical conditions (2 more common causes, 3 rarer causes)
= alcohol
= Viral hepatitis (C > B)
= primary biliary cirrhosis
- haemochromatosis
- A1-anti-trypsin deficiency
- diabetes mellitus
CHOLANGIOCARCINOMA
- most common cause? 1
- what are findings of LFTs?
- management?
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
Presentation of primary liver tumours:
- localised signs / symptoms? 3
- systemic signs / symptoms? 3
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)
HEPATOCELLULAR CARCINOMA:
- what tumour marker to do?
- what other specific blood tests to do? 2 (excl LFTs)
- what investigation to AVOID? 1
- management?
↑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
EPIGASTRIC HERNIA
- location?
- what herniates through where?
- risk factors?
- management options? 2
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
COLONIC POLYPOSIS
- what does polyposis actually mean?
- what condition does this most characteristically occur in? 1
- other conditions it can occur in?
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.
FAP (familial adenomatous polyposis)
- inheritance pattern?
- common age of colon cancer?
- monitoring provided to people found to have?
- prophylactic management options?
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)
Presentation of primary liver tumours:
- localised signs / symptoms? 3
- systemic signs / symptoms? 3
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)
HEPATOCELLULAR CARCINOMA:
- what tumour marker to do?
- what other specific blood tests to do? 2 (excl LFTs)
- what investigation to AVOID? 1
- management?
↑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
ANAL cancer DDx? 5
- perianal warts
- leukoplakia
- lichen sclerosis
- bowen’s disease
- crohn’s disease
FAP (familial adenomatous polyposis)
- inheritance pattern?
- common age of colon cancer?
- monitoring provided to people found to have?
- prophylactic management options?
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)
PERIANAL HAEMATOMA
- management options? 2
leave to resolve spontaneously
OR
evacuated under local anaesthetic
ANAL cancer
- symptoms? 6
- bleeding
- pain
- altered bowel habit
- pruritis ani
- masses
- strictures
ANAL cancer DDx? 5
- perianal warts
- leukoplakia
- lichen sclerosis
- bowen’s disease
- crohn’s disease
FISTULA-IN-ANO
- two types? (categorised by location)
- management of each type?
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
REFEEDING SYNDROME
- briefly describe pathophysiology (incl main ion/electrolyte involved!)
- groups of pts most at risk? 5
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
REFEEDING SYNDROME
- symptoms / features?
HYPO-PHOSPHAETEMIC state norm occurs within 4 hrs
->
- rhabdomyolysis
- red + white cell dysfunction
- respiratory insufficiency
- arrythmias
- cardiogenic shock
- seizures
- sudden death
REFEEDING SYNDROME
- management? 2 (2 things to do, 1 group of things to monitor)
- other health professional to be involved?
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
define these terms:
- dysphagia
- odynophagia
- globus
- dyspepsia
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)
REFEEDING SYNDROME
- briefly describe pathophysiology (incl main ion involved!)
- groups of pts most at risk? 5
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
REFEEDING SYNDROME
- symptoms / features?
h
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
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)
DYSPHAGIA:
- meaning?
DIFFERENTIAL DIAGNOSES:
- mechanical cause? (1 malignant, 2 benign strictures, 3 external pressure, 1 other)
- motility disorders? 4
- other? 2
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
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?
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
What two systemic conditions should you look for if have a pt with dysphagia (one is single condition, one is group of conditions)
1) systemic sclerosis
2) CNS disease
- eg parkinsons, myasthenia gravis etc
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
FBC (anaemia for Ca)
U+E (dehydration)
CXR (mediastinal enlargement, lung Ca)
1) Upper GI endoscopy + biopsy
2) barium swallow
DYSPEPSIA
- featuress of dyspepsis? (4 symptoms, 1 sign)
EPIGASTRIC PAIN
- related to hunger, specific foods or time of day
+/- BLOATING
FULLNESS after meals
HEARTBURN (retrosternal pain + reflux)
TENDER EPIGASTRIUM
DYSPEPSIA
- differential diagnoses? 5
what other groups of causes should you rule out? 3 (esp if epigatric pain predominant symptom)
- 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)
DYSPEPSIA
- associated symptoms to ask about? (6, mneumonic)
ALARMS symptoms
A = Anaemia L = Loss of weight A = Anorexia R = recent onset / progressive symptoms M = Meleana / haematemesis S = Swallowing difficulty (dysphagia)
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?
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
FAECAL INCIONTINENCE
- three groups of causes 3 (give at least one example for each)
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
FAECAL INCONTINENCE
- two body systems to examine? 2 (incl add on test)
- when is faecal incontinence a red flag? what for?
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!
RECTAL BLEEDING:
- what % are caused by UPPER GI bleeds?
- LOWER GI causes? 8
this is FRESH rectal bleeding (ie not meleana)
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)
Most common cause of meleana?
UPPER GI bleed
difference between mesenteric ischaemia and ischaermic colitis?
describe difference in pathology and clinical presentation
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
RECTAL BLEEDING
- add-on examination to always do? 1
- bedside test to do? 1
- bloods to do? 8
- imaging to consider? 2
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
What are the five main groups of causes of abdominal distension? 5
(incl way to remember)
“the 5 Fs”
- Fluid
- Flatus
- Faeces
- Fat
- Foetus
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
- ascites
- bladder (retention)
- large AAA
SHIFTING DULLNESS
If abdominal distension present:
- what should you always ask a woman? 1
- imaging to consider? 2
- other test to consider if suspect ascites? 1
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
JAUNDICE:
- three groups of causes? which are conjugated and which unconjugated hyperbilirubinaemia?
1) PRE-HEPATIC
- unconjugated
2) INTRA-HEPATIC
- mainly conjugated (may be some unconjugated)
3) POST-HEPATIC
- conjugated
Most common aetiology of PRE-hepatic jaundice? (list some examples)
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)
Causes of INTRA-hepatic jaundice? (5 common, 7 rarer)
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
Causes of POST-hepatic jaundice? (aka cholestasis)
- autoimmune? 2
- bile duct obstruction? (2 copmmon, 4 rarer)
- iatrogenic causes to consider? 1
- 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
What other associated symptoms should you ask about if a patient is presenting with jaundice:
- local GI? 5
- systemic? 7
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)
What sign do you look for on examination for cholecystitis? how is this elicited?
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)
common GI causes of vomiting? 7
nb this is in adults, kids can vomit with anything!
= 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)
NON-GI causes of vomiting:
- alcohol + drugs? (3 main, 2 others)
- CNS? (3 main, 3 others)
- metabolic / endocrine? (5 main, 1 other)
- psych? 3
- others? (3 main, 1 other)
nb this is in adults, kids can vomit with anything!
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
VOMITING:
- what to ALWAYS ask if someone vomiting?
- what to ask if female?
what vomit LOOKS like!
- what ate?
- billious? (green)
- frank blood?
- coffee ground?
- feculent? (small bowel obstruction)
ask about possibility of pregnancy!!!
DDx made more likely by TIMING of vomiting:
- morning? 2
- 1hr post food? 1
- vomiting that relieves pain? 2
- vomiting preceeded by loud gurgling?
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)
What associated symptoms to ask about if someone vomiting:
- GI? 5
- systemic? 7
what to clinically assess for?
- abdo pain
- abdo distension
- when last opened bowels?
- passed FLATUS?
- passing urine?
AW FS FIN for systemic
assess for signs of DEHYDRATION hydration status
Investigations to consider for vomiting:
- bloods?
- if suspect obstruction? 1
- if suspect raised ICP? 1
- on all pre-menopausal females? 1
- to consider if persistent vomiting? 1
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
What electrolyte abnormality can be seen in severe vomiting?
what other abnormality may be seen on the gas?
- why might you get a urine dip in severe vomiting?
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)
ANTIEMETICS:
- that target histamine (H1) receptors? (1 most common, 1 other)
- that target dopamine (D2) receptors? 4
- that target serotonin (5HT3) rectors? 1
- other drugs with anti-emetic properties? 3
for each of these list generally what causes of N+V they should be used for?
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)
ANTIEMETICS:
- who should you avoid cyclizine in? 1
- who should you avoid metoclopramide and other dopimergic drugs in? 2
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
DIABETIC FOOT DISEASE
- pathology (describe the 2 main mechanisms)? 2
- how do you screen for each of these two pathologies? 2 (who should have regular follow up at diabetes foot centre - ie more than just screening?)
- describe clinical presentation of each? 2 (nb not of complications!)
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
How to tell difference between venous, arterial and neuropathic ulcers?
incl location, pain etc
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
DIABETIC NEUROPATHIC ARTHROPATHY:
- aka?
- describe pathology?
- describe presentation?
- management?
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
Management of complications of diabetic foot disease:
- how to prevent? 1
- imaging if any ulcers / deformities? 1
- management of diabetic foot ulcers?
- who to refer to if can’t feel pulses?
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
GRAVES DISEASE
- what % of hyperthyroidism?
- other causes of primary hyperthyroidism? 3
- pathophysiology?
- gender + age most affected?
- what conditions associated with?
- common triggers? 3
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
What is meant by ‘subclinical’ hypo and hyperthyroidism?
how are these managed?
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!
THYROID ANTIBODIES
which condition out of:
- grave’s
- hashimoto’s
- thyroid cancer
- postpartum thyroiditis
are these most likely to be present in:
- TSH receptor antibodies (TRAb)
- Thyroid peroxidase antibodies (TPOAb or anti-TPO)
- Thyroglobulin antibodies (TgAb)
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
GRAVES DISEASE
- describe palpation findings of the thyroid gland?
- additional signs / conditions found in graves disease? 4 (ie not found in other causes of hyperthyroidism)
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
SUSPECTED HYPERTHYROIDISM
- 1st line bloods? 2
- 2nd line bloods to do? 1
- other investigations to consider? 2
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!
GRAVES DISEASE
- symptomatic mx? 1
- 1st line? 1 (what if pregnant? 1)
- options if relapse? 2
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!)
CARBIMAZOLE
- main adverse effects? 3
- agranulocytosis
- teratogen (make sure on contraception)
- cholestatic jaundice (? is this one right? **)
THYROID EYE DISEASE
- biggest modifiable risk factor? 1
- symptoms / features?
- when to refer to opthalmology?
- management? 3
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!
THYROTOXIC CRISIS / STORM
- who gets it?
- triggers? 5
- clinical features? 4
- change in obs? 3
- 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!!
MANAGEMENT OF THYROID STORM:
- to reduce temp? 1
- to slow heart? 1
- anti-thyroid drug? 1 (be specific)
- other drugs? 2
- who to consider calling for help? 1
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!
BIGUANIDES
- example?
- brief mechanism of action?
- gain or loose weight?
- contraindications? 2
- adverse effects? 2
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
OTHER ORAL MEDS FOR T2DM
for each:
- example?
- brief mechanism of action?
- gain or loose weight?
- Sulfonylureas
- Glitazones
- Gliptins
- GLP-1 mimics
- SGLT-2 inhibitors
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
OTHER ORAL MEDS FOR T2DM
for each:
- example?
- contraindications?
- adverse effects?
- Sulfonylureas (3 CI, 2 AE)
- Glitazones (4 CI, 3 AE)
- Gliptins (3 CI, 4 AE)
- GLP-1 mimics (3 CI, 2 AE)
- SGLT-2 inhibitors (3 CI, 4 AE)
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
ADRENOCORTICAL INSUFFICIENCY:
- what two groups of hormones are deficient?
- what electrolyte effects does this have?
↓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)
What does aldosterone (mineralocorticoid) do?
incl effect on BP, Na and K
Increases BP by retaining salt (and thus excreting K+)
What happens to:
- BP
- Glucose
- Sodium
- Potasium
in:
- Addisons
- Cushings
- Conns
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!
ADRENOCORTICAL INSUFFICIENCY:
- most common cause (of primary and overall)? (gender and age most affected?)
- other causes of primary? 5
- groups of secondary causes? 2
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
ADDISON’S
- symptoms + signs?
- which sign is NOT present in secondary adrenal insufficiency
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
ADDISONS:
- initial blood test to do for screening? 1
- other bloods to do? 4
- diagnostic test? 1
- what can you do to exclude secondary causes? 1
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
ADDISONS:
- two key meds for management?
- additional instructions to give for when pt is unwell?
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)
ADDISONIAN CRISIS
- THREE main features?
- THREE key things for management? 3 (+ way to remember!)
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
HYPOTHYROIDISM
- most common cause of primary?
- other causes of primary? 7
- which of these have an initial hyperthyroid phase? 2/3
- medications which can cause hypothyroidism? 3
- most common cause of secondary hypothyroidism?
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
HASHIMOTO’S THYROIDITIS
- gender most affected?
- autoimmune conditions associated with? 3
- non-autimmune conditions associated with? 3
Female (5-10 times more common)
- type 1 DM
- addison’s
- perncious anaemia
- Down’s syndrome
- Turner’s syndrome
- coeliac disease
HYPOTHYROIDISM
- typical symptoms?
- typical signs?
- 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
HYPOTHYROIDISM
- investigations? 3
- what used for monitoring? 1
- management? 1
- possible side effects of treatment? 4
- 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
MYXOEDEMA COMA
- who does this occur in?
- two main features? 2
- management? 4
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
SICK EUTHYROID SYNDROME
- what is it?
- what happens to TFTs?
- management?
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
HYPERPARATHYROIDISM:
- ways in which PTH increases blood calcium? 3
- describe difference between primary, secondary and tertiary hyperparathyroidism?
incl calcium and PTH levels
- COMMONEST cause of PRIMARY hyperparathyroidism?
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!
HYPERPARATHYROIDISM
- commonest cause of primary? 1
- other causes of primary? 3
- commonest cause of secondary? 1
- other causes of secondary? 3
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!
Symptoms of HYPERCALCAEMIA:
- stones? 1
- bones? 5
- abdominal groans? 5
- thrones? 1
- psych overtones? 4
- others? 3
which of these norm happen first? 2
what ECG abnormality can you sometimes see? 1
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
PRIMARY HYPERPARATHYROIDISM:
- bloods to do if suspect? 4 (+ findings)
- conservative management to lower calcium levels? 1
- which med to AVOID? 1
- definitive management? 1
- what is sometimes used if person is unfit for surgery? 1
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!
Main differential for primary hyperparathyroidism?
how does it mimic?
Malignancy
parathyroid related protein is produced by SCC lung cancer (breast and renal too) → mimics PTH → high calcium!
Management of secondary hyperparathyroidism:
- main focus? 1
- additional meds that may be used? 2
TREAT UNDERLYING CONDITION (ie norm CKD)
- phosphate dietary restriction +/- phosphate binders
- activated vit D (if deficienct)
Management of tertiary hyperparathyroidism?
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.
HYPERLIPIDAEMIA
- acquired causes of predominantly high triglycerides? 5
- medication causes of high triglycerides? 3
- acquired causes of predominantly high cholesterol? 3
- inherited cause of hyperlipidaemia? 1
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
HYPERLIPIDAEMIA
- how most picked up?
- signs on examination that may see? (3 skin, 1 eye)
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)
HYPERLIPIDAEMIA
- what bloods to do? 1
- bedside tests to do if suspect? 2
- lifestyle advice for all? 3
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)
QRISK2 SCORE
- who should it be used in?
- what % level should you offer a statin?
- who else should get 20mg statin? 3 (ie without doing QRISK2 score)
- who should get 20mg statin? 3
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
HYPOPARATHYROIDISM:
- causes of primary? 3
- what is pseudohypoparathyroidism?
- what is pseudopseudohypoparathyroidism?
- 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
Main symptoms of hypoparathyroidism? 3
- what are these due to? 1
- two clinical tests/signs? 2
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)
POSSIBLE finding on ECG if:
- low calcium?
- high calcium?
low calcium = prolonged QT interval
high calcium = shortened QT interval
HYPOPARATHYROIDISM
- bloods to do? 4 (+ findings in primary + pseud)
- others to consider to find cause? 2
- other investigations to do if suspect pseudohypoparathyroidism? 2
- management? 1
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?
THYROID CANCER TYPE
which most common?
papillary
- age group?
- histology?
- Mx?
follicular
- age group?
- histology?
- Mx?
medullary
- main risk factor?
- what may produce?
- Mx?
anaplastic
- age group?
- often present with?
- prognosis?
lymphoma
- main risk factor?
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
THYROID CANCER
- how present?
- possible late features? 5
- 1st line investigation for all
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!
TOXIC MULTINODULAR GOITRE
- how does it present?
- main risk factors? 2
- what develop from? 1
- finding on nuclear scintigraphy? 1
- management options? 2
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!
TOXIC THYROID NODULE / ADENOMA
- how present?
- age and gender most affected?
- finding on nuclear scintigraphy? 1
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!
GOITRE
- causes of diffuse? (2 hyperthyroid, 3 hypo, 1 euthyroid)
- causes of nodular? (2 hyper, 3 euthyroid)
1st line investigations for a goitre? 2
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
What local obstructive symptoms may occur with a goitre? 2 main groups
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!
HYPOPITUATIRISM
- which hormones can be affected? 5
- what syndrome does each of these hormone deficiencies cause?
- what hormones could be affected if really bad? 2
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)
GROWTH HORMONE DEFICIENCY
- presentation in children?
- presentation in adults?
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!
SECONDARY HYPOGONADISM
- how present in women?
- how present in men?
WOMEN
- Oligomennorhoea or Amenorrhoea
- ↓Fertility, ↓Libido, Dyspareunia
- Breast atrophy
MEN
- Erectile dysfunction
- ↓muscle bulk
- Hypogonadism (↓hair, small testes, ↓ejaculate vol, ↓sperm)
HYPOPITUATIRISM
- if cause is gradual what is the normal order in which hormones are affected?
- so what is the most common presenting symptom in adults? (1) and children? (1)
nb this doesn’t apply if the cause of hypo pit is acute!
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
HYPOPITUATIRISM
- compressive causes? 5
- other causes? 4
- commonest of these causes? 1
nb compressive is my word, can’t think of a better one… but basically stuff that compresses the pituatory gland and so reduces it’s hormone prioduction / release
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!)
PITUATORY ADENOMA
- difference between a macroadenoma and microadenoma?
- other way of defining?
- most common type?
- 2nd most common type?
- 4 other rarer types?
^briefly describe each/effect of hormones
^nb clue: just think of hormones the anterior pituatory releases!
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
PITUATORY ADENOMA
- three main groups of symptoms / ways they present?
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)
Investigaitons for suspected pituatory adenoma:
- group of bloods?
- other tests? 2
- management options? 3
- what’s 1st line Mx for prolactinoma? 1
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
describe clinical presentation of Acromegaly?
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!
SUPPRESSED HYPOTHALAMO-PIT-ADRENAL AXIS
- most common cause? (describe pathology)
- how does it present clinically?
- how to prevent?
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!
PHAEOCHROMOCYTOMA
- describe it?
- tumour syndromes associated with? 3
- what % are bilateral, malignant and extra-adrenal?
- main symptoms? 4
- main finding on obs? 2
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
PHAEOCHROMOCYTOMA
- main investigation? 1
- intermediate management? 2
- definitive management? 1
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!
CUSHING’S SYNDROME
- main cause of ACTH independent? 1 (3 other causes?)
- two main cause of ACTH-dependent?
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%)
CUSHING’S SYNDROME
- symptoms? 5
- what MSK complications at risk of? 2
↑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…
CUSHING’S SYNDROME
- signs? 4
- what may see on blood gas?
- 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
CUSHING’S SYNDROME
- 1st line test? 1
- next 2 tests if that suggests it’s ACTH dependent? 1
(also describe findings)
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
PSEUDOCUSHINGS
- what is it? (incl cause)
- how to differentiate between this and true cushings?
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
PRIMARY HYPERALDOSTERONISM
- two commonest causes?
- how present?
- K+?
- Na?
- blood gas?
- 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+
PRIMARY HYPERALDOSTERONISM
- diagnostic investigation? 1
- additional investigation to find cause?
- management for two main causes?
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
SECONDARY HYPERALDOSTERONISM:
- pathophysiology?
- causes? 5
- findings on investigations?
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!
HYPOALDOSTERONISM
- most common cause?
- what DON’T you get it in!
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!
Difference between hirsutism and hypertrichosis?
ie define them both
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)
HIRSUTISM
- Commonest cause?
- other causes?
- what drugs can cause it? 2
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
HIRSUTISM
- what can be used to assess severity?
- lifestyle advice? 1
- possible symptomatic management? 3
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!!!!
DIABETES INSIPIDUS:
- two types? (describe pathology of how these cause symptoms!)
- give examples of causes of each (don’t worry too much about these)
- main symptoms? 2 (regardless of type)
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)
DIABETES INSIPIDUS
- main DDx?
- investigation to diagnose? 1
- investigation to differentiate between neurogenic and nephrogenic?
- Mx for two different types? (2 nephro, 1 neuro)
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+)
SIADH
- describe pathophysiology?
- what electrolyte imbalance does it cause?
- main investigation? 1 (findings?)
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!
causes of SIADH
- malignancy? (1 main, 2 rarer)
- neurological? 4
- infections? 2
- medications? (2 anti-D, 1 anti-epileptic, 2 chemo, 1 DM med)
- other causes (2, both rare)
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
SIADH management? 2 (1 action, 1 med)
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
GYNAECOMASTIA
- what is is? and what important to differentiate from?
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
CAUSES of GYNAECOMASTIA
- physiological cause?
- causes dt low testosterone? 2
- causes dt higher oestrogen? 1
- other causes? 4
nb see other flashcard for medication causes
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
MEDICATION CAUSES of GYNAECOMASTIA
- most common cause? 1
- others? (1 H2 antagonist, 1 heart med, 1 prostate med, 2 recreational, 2 others)
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
Differential diagnosis for POLYURIA (+/- polydipsia)? (2 endocrine, 1 metabolic, 2 other, 1 med)
1st line investigation?
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!)
HYPONATRAEMIA
if you find low sodium on a blood test, what are the THREE things you need to assess / measure?
when do you delay doing these investigations?
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)
CAUSES of HYPOTONIC HYPONATRAEMIA (ie TRUE low sodium - also have a low serum osmolarity!)
- group of causes with HYPOvolaemia AND HIGH urine osmolarity/Na? 1 (give examples)
- group of causes with HYPOvolaemia AND LOW urine osmolarity/Na? 1 (give examples)
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
CAUSES of HYPOTONIC HYPONATRAEMIA (ie TRUE low sodium - also have a low serum osmolarity!)
- causes with EUvolaemia AND HIGH urine osmolarity/Na? 4
- causes with EUvolaemia AND LOW urine osmolarity/Na? 4
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
CAUSES of HYPOTONIC HYPONATRAEMIA (ie TRUE low sodium - also have a low serum osmolarity!)
- MAIN cause with HYPERvolaemia AND HIGH urine osmolarity/Na? 1
- causes with HYPERvolaemia AND LOW urine osmolarity/Na? 3
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
Management of HYPONATRAEMIA
- what three things do you need to know in order to choose your management plan? 3 (ie choose how aggressively to treat)
^this is nothing to do with causes!
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!
HYPONATRAEMIA
for:
- mild
- moderate
- severe
list:
- serum Na level
- symptoms
- management (2 mild, 3 mod, 2 severe)
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!
HYPONATRAEMIA
- how fast can you correct if acute? (<48hrs)
- how fast can you correct if chronic? (>48hrs or unknown)
ACUTE
- max 1mmol/hr (24mmol/day) (check w senior first!)
CHRONIC
- max 10mmol/day
ie do repeated U+Es to check!!
