Med 2 LOs Flashcards

Question 1

Q

risk factors for peptic ulcer disease

Answer

A

Infection by H. Pylori
Medicines
- NSAID’s- nurofen, ibuprofen, diclofenac
- Oral corticosteroids
- SSRIs
- Bisphosphonates- to fight osteoporosis
- Potassium chloride
- Chemotherapy drugs
Health problems
- Cytomegalovirus infection
- Crohn disease
Other factors
Smoking
Drinking alcohol
Having type O blood
Having other family members with peptic ulcer disease

Question 2

Q

Symptoms of peptic ulcer disease

Answer

A

Burning stomach pain that:
- May wake someone during sleep
- Last mins- hours
- Is worse with an empty stomach and better after eating or drinking
- Feels better after having antacids
Nausea
Lack of hunger
Burping
Bloating
Feeling of fullness after meals
Heartburn
Ulcers can cause bleeding. It is rare can cause:
- Melaena (black, tarry stools)
- Haematemesis- Coffee ground vomit

Hypotension, tachycardia

Question 3

Q

differential diagnosis peptic ulcer

Answer

A

GORD

gastritis

oesophageal varicoeal bleed

sleep apnoea

Question 4

Q

which artery is most likely to be eroded in peptic ulcer disease

Answer

A

gastroduodenal artery

Question 5

Q

investigations for peptic ulcer disease

Answer

A

Endoscope
Carbon-13 urea breath test for H. Pylori
Stool antigen test (as long as no PPI in 2 weeks or antibiotic in 4)
CXR- look for air under left side of diaphragm

Question 6

Q

management of peptic ulcer disease

Answer

A

ABC approach as with any upper gastrointestinal hemorrhage
First line treatment is endoscopic intervention
Stopped medication contributing to dyspepsia
Interventional angiography with transarterial embolization or surgery
If H. pylori +ve - 1 IV proton pump inhibitor (osemoprazole, lansoprazole) + 2 Antibiotics (amoxicillin, clarithromycin, metronidazole, tetracycline)
If H.Pylori -ve –> acid suppression alone
If intolerant to PPI try H2RA- ranitidine

Question 7

Q

Outline the fluid management of a patient with a GI haemorrhage.

Answer

A

Get IV access

Begin fluid resuscitation immediately

500mL of normal saline or lactated Ringer’s solution over the first 30 mins

Cross-match for transfusion

Endoscope to determine whether variceal bleed or not- if variceal give antibiotic prophylaxis and terlipressin

Question 8

Q

differential diagnosis for someone with GI bleeding

Answer

A

Peptic ulcer (H. pylori, medication, ZE syndrome)
Mallory Weiss tear (binge drink and then vomit)
Oesophageal variceal hemorrhage (secondary to liver disease)
Gastritis
Drugs–> NSAID’s, steroids
Neoplasms (gastric cancers)
Surgical failure
Oesophagitis
Oesophageal cancer
AAA

Question 9

Q

How would you assess the risk of an upper GI bleed?

after an endoscope how would you assess risk of rebleed or mortality

Answer

A

Blatchford score

first assessment
done to assess the likelihood that someone with an upper gI bleed will need to have medical intervention such as a transfusion or endoscope

Rockall score- after endoscopy. Used to reassess risk of rebleeding and mortality

Question 10

Q

how would you rescuscitate someone after an upepr GI bleed?

Answer

A

Protect airway and give high flow oxygen
Large bore cannula and take FBC, LFT, U+E, cross match
500 ml over 15 mins then another 500ml over the next 45 mins
Transfuse with blood (O if specific not known), platelets (if <50 x10^9/L)
Platelets –> fresh frozen plasma (if prothrombin time >1.5 normal) –> cryoprecipitate
Catheterise and monitor hourly urine output
Suspicion of varices then give terlipressin + IV broad spectrum
Arrange urgent endoscopy

Question 11

Q

ways of treating an upper GI bleed with an endoscope

non-variceal bleed
variceal bleed

Answer

A

non-variceal bleed

endoscopic treatment

mechanical method (e.g., clips) with or without adrenaline
thermal coagulation with adrenaline
fibrin or thrombin with adrenaline

PPI

variceal bleed

terlipressin (casues vasoconstriction of the splenic artery, reducing BP in portal system)

prophylactic antibiotic treatment

oseophageal varices

band ligation

TIPS- transjugular intrahepatic portosystemic shunts if above methods failure

Gastric varices

N-butyl-2-cyanoacrylate

TIPS- transjugular intrahepatic portosystemic shunts

Strict fluid monitoring

Prophylactic

Question 12

Q

by quadrant or area of the abdomen list what could cause pain

Question 13

Q

Physiology of vomiting

Answer

A

Reflex expulsion of gastric (and sometimes intestinal) contents- reverse peristalsis and abdominal contraction.

Vomiting centre in part of the medulla oblangata called the area prostrema and is triggered by receptors in several locations:

Labyrinth receptors of ear (motion sickness)
Overdistension of receptors of duodenum and stomach (communicates via tractus solitarius- vagal sensory tract)
Trigger zone of CNS- e.g., drugs like opiates act here
Touch receptors in throat

Causes of vomiting

Gastritis
GORD
Peptic ulcer disease
Acute gastroenteritis

Question 14

Q

Question 15

Q

differential diagnosis for. aptient with a change in bowel habit

Answer

A

IBD
Crohn’s disease
Ulcerative colitis
Hypo/hyperthyroidism
Coeliac disease
Bowel cancer
Milk intolerance
Gatroenteritis
Food poisoning
Meleana- peptic ulcer disease
Steatorrhea- cystic fibrosis, liver damage, gallstones
Diverticulosis
Antibiotics
Spinal cord injury/ nerve damage affecting sphincter control

Question 16

Q

Which blood results can be used to interpret the coagulability of blood

Answer

A

Prothrombin time (PT)

APTT

INR

FBC

Albumin

D/dimer

Question 17

Q

what is prothrombin time

Answer

A

A measure of the time taken for a blood clot to form via the extrinsic pathway (factors V11, X,V and II). Play Tennis OUTSIDE.
Healthy is 12-14 seconds

Question 18

Q

what is APTT

what diseases are likely to cause a change in it?

Answer

A

activated partial prothromboplastin time

35-45 seconds

Measure of time taken for blood to clot via intrinsic pathway (XII, XI, IX, X,V and II)

Affected by clotting factor synthesis or consumption

The main factors that may alter it are

Haemophilia A (VIII – X-linked recessive)
Haemophilia B (IX – X-linked recessive)
Haemophilia C (XI – autosomal recessive)
von Willebrands disease (as vWF pairs up with factor VIII)

Question 19

Q

What is INR

Answer

A

Standardised version of PT.

Commonly used on patients who use anticoagulants- e.g., warfarin

INR= patient PT/ control PT

This test can be affected by: liver disease (decrease) , disseminated intravascular coagulation (increase), vitamin K deficiency (increase) and warfarin levels (increase).

Question 20

Q

How would each of these conditions/ changes affect PT/INR APTT and platelet count

Vitamin K deficiency/ warfarin use
Haemophilia A/B/C (clotting disorder- haemarthrosis (bleeding and pain into unilateral joint), muscle haematomas
Von Willebrand disease (symptoms of platelet disorders- petechiae, bruising, contact bleeding e.g., gums, menorrhagia
DIC (Disseminated Intravascular coagulation): (total coagulopathy, give platelets and clotting factors)
ITP, TTP, HUS don’t give platelets to these patients

Answer

A

Vitamin K deficiency/ warfarin use
- PT/INR increase APTT inrcease platelet count –
Haemophilia A/B/C (clotting disorder- haemarthrosis (bleeding and pain into unilateral joint), muscle haematomas
- PT/INR- APTTincrease platelet count -
Von Willebrand disease (symptoms of platelet disorders- petechiae, bruising, contact bleeding e.g., gums, menorrhagia
- PT/INR- APTT increase/- platelet count-
DIC (Disseminated Intravascular coagulation): (total coagulopathy, give platelets and clotting factors)
- PT/INR increase APTT increase platelet count ¯
ITP, TTP, HUS don’t give platelets to these patients
- PT/INR - APTT- platlet count decrease

Question 21

Q

What is haemophilia
is it inherited or acquired?
which gender is more at risk?
What is the inheritance pattern?
which gene is most commonly affected?

Answer

A

usually an inhertied bleeding disorder
may be acquired because the liver produces clotting factors. vitamin K deficiency can also cause haemophilia
men are more at risk because the mutated genes associated with H A and B are both found on the X chromosome, making it an X linked condition
each son of a carrier has a 50% chance of having the disease
genes F8 and F9 are the most fequently affected genes

Question 22

Q

Haemophilia A

Answer

A

Factor 8 deficiency

80% of haemophilias

Levels may also be lower in von Willenbrand disease -look also at that

Question 23

Q

Haemophilia B (Christmas disease)

Answer

A

factor 9 deficiency

Question 24

Q

Signs and symptoms for haemophilia

Answer

A

Nearly identical for 8 + 9

Easy bruising (ecchymosis)
Haematoma (collections of blood outside of the vessels)
Prolonged bleeding after cut or incisison
Oozing after tooth extractions
GI bleeding
Severe nosebleeds
Haemarthritis (bleeding into joint spaces)
Bleeding into brain  stroke or increased intracranial pressure

Question 25

Q

diagnosis of the haemophilias

treatment

Answer

A

platelets normal
Prothrombin time –> tests EXTRINSIC –> normal
APTT –>tests INTRINSIC and therefore F8 + F9 –> prolonged
confirmation–> genetic testing + assays of the factors

treatment

Injections of missing or non-functional clotting factor

Question 26

Q

vitamin K deficiency

which vitamins are fat soluble

causes of K deficiency

Answer

A

Vitamins ADEK are fat soluble so without bile they cant be absorbed by the intestines. eaten in leafy greens

causes of vit K deficiency

Lack in diet
Very low fat diet
Disorders that stop fat absorption–> blockage of bile duct, cystic fibrosis, liver disease, coeliacs
Newborns are prone to it

Question 27

Q

symptoms of vitamin K deficiency

treatment

Answer

A

haemorrhage- epistaxis, sound, GI malaena
easily bruises
small clotes under the nails

phytonadione

Question 28

Q

Von Willebrand disease

what does vWf do?

Answer

A

Decrease in quality or quantity of von Willebrand factor

Binds and carries factor 8 (protects from protein C and S that would degrade it too early)

Inherited

type 1 autosomal dominant
type 2 not high enough quality vWF
type 3 autosomal recessive, most dangerous, no VWF and very low F8

Question 29

Q

vWillebrand disease

symptoms

diagnosis

which antibiotic can cause it

Answer

A

symptoms of vWf deficiency

Depends on type
Severe type 3–> joint and GI bleeding
Acquired–> new onset bleeding following recent disease or new medication

diagnosis

PT/INR - APTT increased. platelet count -

vWF antigen in blood

Question 30

Q

Form a differential diagnosis for someone presenting with tiredness

<1 month

chronic

Answer

A

Lasting <1 mo

Drug adverse reavctions (antidepressants, antihistamines, antihypertensives, hypokalemic diuretics
Anaemia
Stress/ depression - anhedonia?
Hypercalcaemia

Chronic disorders

Diabetes
Hypothyroidism
Sleep disturbances (apnoea)
Cancer
CKD
SLE

Endocrine

Adrenal insufficiency
Diabetes
Pituitary insfufficiency

Infections

Cytomegalovirus infection
Endocarditis
Hepatitis

Question 31

Q

diabetes

which population is type 1 more frequent in?

complications of both types of diabetes?

Answer

A

T1DM more common in caucasian populations

Seen in poorly controlled diabetes

Microvascular:

Retinopathy
Nephropathy
Neuropathy

Skin healing impairments - ulceration

Macrovascular:

Involves atherosclerosis of large vessels
Angina
MI
TIA+ stroke
Peripheral arterial disease

Question 32

Q

diagnosis of DM

Answer

A

Persistent hyperglycaemia + clinical features

how to measure peristent hyperglycaemia :

HBA1C of 48 mmol/mol (6.5%) or more
Fasting plasma glucose of 7.0 mmol/L
Random plasma glucose 0f >11.1

Question 33

Q

alternative causes for hyperglycaemia

Answer

A

Pancreatic disease: CF, pancreatitis, haemachromatosis, pancreatectomy

Endocrinopathies: cushing syndrome, acromegaly, phaeochromocytoma, hyperthyroidism

Drugs: glucocorticoids, B-blockers, thyroid hormone

Viral infections can also trigger–> cytomegalovirus CMV rubella, RBV

Pregnancy

Question 34

Q

T1DM

AKA?

what % of DM cases?

patho?

epidemiolgy?

associated with what?

Answer

A

Primary insulin insufficiency/ dependent
10% of cases
Autoimmune destruction of beta cells in pancreas
More common in <30-year-olds but can occur in later life
Associated with other autoimmune disorders

Question 35

Q

symptoms of T1DM?

Answer

A

Thirst
Polyuria (weeing a lot)
Weight loss
Lethargy
Nausea
Vomiting
Blurred vision
Polyphagia (intense hunger)
Predisposes you to bacterial and fungal infections
Ketoacidosis
confusion
fruity smelling breath
weakness

Question 36

Q

treatment of T1DM

Answer

A

Exogenous insulin (sub-cut or in emergency IV
Basal bolus regimen- basal injection for day and then boluses as needed
Managing hypos- eating small doses of sugary food to correct
Education

Question 37

Q

T2DM

what % of DM cases?

patho?

linked to what?

acquired or inherited?

causes (2)

Answer

A

90% of all cases
Insulin resistance, ↓insulin secretion and ↑glucagon secretion
Secondary beta cell failure
Linked to obesity
Strong familial tendency
Tends to occur in later life but seen increasingly in children
Gradual onset
Cells in muscle, fat and the liver become resistant to insulin. Because these cells don’t interact in a normal way with insulin, they don’t take in enough sugar.
The pancreas is unable to produce enough insulin to manage blood sugar levels.
Exactly why this happens is unknown, but being overweight and inactive are key contributing factors

Question 38

Q

symptoms of T2DM

Answer

A

Symptoms

Polydipsia
Polyuria
Blurred vision
Unexplained weight loss
Recurrent infections
Tiredness

signs

Acanthosis nigricans: dark pigmentation of skin folds insulin resistance

Presence of risk factors

Question 39

Q

risk factors for T2DM

Answer

A

Obesity and inactivity
Age >45
Sedentary lifestyle
Family history
Ethnicity (Asian, African, afro-Caribbean)
History of gestational diabetes
Diet (low-fibre, high glycaemic index)
Drug treatments (statins, corticosteroids, thiazide diuretic+beta blocker)
Polycystic ovary syndrome
Metabolic syndrome (raised BP, dyslipidaemia, fatty liver disease, central obesity, tendency for thrombosis)

Question 40

Q

treatment for T2DM

Answer

A

Lifestyle (diet + exercise) –> medications –> insulin

Screen for complications 5 year after diagnosis and after that do each test regularly (fundoscopy, foot exam, urine test for albumin, serum creatinine and lipid profile)

Metformin 1^st line- reduces hepatic gluconeogenesis, increase skeletal muscle glucose uptake –> contraindicated in renal problems
Sulfonylureas 2^nd line – gliclazide, glipizide, insulin secretagogue
Thiazolidinediones 3^rd line – pioglitazone
Alpha-glucosidase inhibitors- acarbose
GLP-1 receptor analogues

Question 41

Q

Question 42

Q

how does renal disease present? (2)

Answer

A

asymptomatically
renal tract symptoms

Question 43

Q

how do you detect renal disease in

asymptomatic presentation
renal tract symptoms

Answer

A

1) Asymptomatic disease

Non-visible haematuria
Abnormal renal function test (GFR)
High blood pressure
Electrolyte abnormalities- sodium, potassium, acid-base balance
Proteinuria

2) Renal tract symptoms

Urinary symptoms:

Dysuria
Frequency
Nocturia
(consider prostatic cause if voiding, poor stream and dribbling present)
Oliguria/ Anuria (too little or nothing)  think AKI
Polyuria  DDx diabetes mellitus

Loin pain:

Ureteric colic think kidney stone
Localised pain pyelonephritis, renal cyst pathology, renal infarct

Visible haematuria:

Exclude renal cance
Nephrological casues = polycystic kidney disease, glomerular disease,

Nephrotic syndrome:

Proteinuria (>3g/24Hrs), >300mg/ mmol
- hypoalbuminaemia (<30g/L)
- peripheral oedema

Symptomatic chronic kidney disease:

Dyspnoea
Anorexia
Weight loss
Pruritis
Bone pain
Sexual dysfunction

Question 44

Q

Acute renal disease (AKI)

what is it? how is it measured?

definition by diagnosis?

Answer

A

= acute kidney injury = AKI

Syndrome of decreased renal function, measured by serum creatinine or urine ouput occurring over hours–> days

Definition:

Rise in creatinine of >26mmol/L within 48 hours
Rise in creatinine >1.5 x baseline within 7days
Urine output< 0.5mmol/L/kg/ h for >6 consecutive hours

Question 45

Q

how do you stage an AKI?

risk factors for an AKI

Answer

A

serum creatinine vs urine output

Pre-existing CKD
Age
Male
Comorbidity (DM, cardiovascular disease, malignancy, chronic liver disease, complex surgery)

Question 46

Q

symptoms of an AKI

Answer

A

Most asymptomatic

Confusion
Oliguria – little urination
Listlessness
Fatigue
Anorexia
Nausea
Vomiting
Weight gain
Oedema

Signs of an AKI

Raised BUN- blood urea nitrogen
Raised creatinine
Hypertension
Impaired H+ secretion – alkalosis
Hyperkalaemia
In some cases like HF, pulmonary oedema or huypertension  retain water and sodium – peripheral or periorbital oedema
Lack of erythropoietin anaemia
Hypoclacaemia

Question 47

Q

causes of an AKI

Answer

A

Sepsis
Major surgery
Cardiogenic shock
Other hypovolaemia
Drugs
Hepatorenal syndrome
Obstruction

Question 48

Q

aetiology of an AKI can be split into 3:

Answer

A

Pre-renal: ¯renal perfusion

¯vascular volume (haemorrhage, burns, pancreatitis)

¯cardiac output (cardiogenic shock, MI)

Systemic vasodilation (sepsis, drugs)

Renal; vasoconstriction (NSAIDs, ACE-I, ARB)

Renal: intrinsic renal disease

Glomerular; glomerulonephritis

Interstitial; drug reaction, infection, infiltration (e.g., sarcoidosis)

Vessels; vasculitis

Post-renal: obstruction to urine

Within renal tract; stone, malignancy, stricture, clot

Extrinsic compression; pelvic malignancy, prostatic hypertophy

Question 49

Q

Is someone with diabetes more likely to have nephritic or nephrotic syndrome?

Answer

A

Nephritic

Question 50

Q

Differential diagnoses of an AKI

Answer

A

Chronic kidney disease
Hypoglycaemia DM
Renal calculi
Sickle cell anaemia
Dehydration
GI bleed
Heart failure
UTI
Protein overload
DKA
Urinary obstruction

Question 51

Q

Investigations of AKI

Answer

A

Urine dip–> quantification of proteinuria/ haematuria
Renal USS within 24hrs–> check LFT–> hepatorenal disease
Check for platelets–> if low consider blood film
Investigate for intrinsic disease–> e.g., immunoglobulins and paraprotein from myeloma
Nephritis—white cell casts

Question 52

Q

U&Es for kidney injuries/ dysfunction

Answer

A

High potassium, high creatinine and high urea

Question 53

Q

what are 2 examples of acute renal diseases?

Answer

A

Nephrotic syndrome

Diabetic Nephropathy

Question 54

Q

nephrotic syndrome

triad of:

commonest cause in young people?

Answer

A

presents with the classic triad of:

Proteinuria (>3.5g/24Hrs shouldn’t have any if healthy), >300mg/ mmol
+ hypoalbuminaemia (<30g/L)
+ peripheral oedema

may also see hypercoagulability

Commonest cause in a young person–> autoimmune

Question 55

Q

Aetiology of nephrotic syndrome

primary renal and secodnary to systemic

Answer

A

Primary renal disease-
- Minimal change- commonest in kids
- Membranous nephropathy - commonest in adults, protein build up on basement membrane
- Focal segmental glomerulosclerosis
Secondary to systemic disorder
- Pre-eclampsia (more relevant to HELLP)
- Lupus nephritis (butterfly rash on face)
- Protein deposition diseases (myeloma, amyloidosis)
- Diabetes
- Cancer
- Infections (Hep B, HIV)
- Genetic conditions
- NSAID’s

Question 56

Q

presentation of nephrotic syndrome

Answer

A

a) Symptoms

Periorbital oedema–> Dependant oedema–> altered by gravity (as someone lies overnight their eyes get puffy but drains as he stands and walks) (as you walk around during the day your feet swell)
Pitting oedema
Weight gain
Frothy urine
Symptoms of cause–> infection

b) Signs

Raised jvp?
Hypertension
Hyperlipidaemia xanthelasma

Question 57

Q

investigations for nephrotic syndrome

Answer

A

Obs–> BP–> hypertension
Urine–> dipstick (looking for nitrates, proteins etc.) + look for culture (infective cause) + 24hr urine collection + creatinine: albumin
LFT–> look for hypoalbuminaemia
U+E–> check kidney function –> high urea in dysfunction
USS–> may show scarred kidney or polycystic kidney
Renal biopsy–> looking for glomerular sclerosis (minimal change)

24hr urine collection

Question 58

Q

management of nephrotic syndrome

Answer

A

Reduce oedema
1. fluid and salt restriction
2. diuresis with loop diuretics e.g., furosemide (be careful in people with renal failure)
3. aim for 0.15kg–> 1kg weight loss per day
Treat underlying cause
1. Renal biopsy
2. Steroids
Reduce proteinuria
1. ACE-i/ ARB reduces proteinuria
Manage complications–> e.g., give anticoagulants
Immunosuppression –> for causes like lupus???

Question 59

Q

complications of nephrotic syndrome

Answer

A

Malnutrition–> nephrotic for a long time
Thromboembolism
Infection (urine losses of immunoglobulins)
Hyperlidipaemia –> increased cholesterol + ↑triglyceridemic
AKI/ CKI Renal failure → hyperkalaemia
Hypertension

Question 60

Q

diabetic nephropathy

commonest cause of end stage renal failure

diagnosis:

treatment:

Answer

A

Diagnosis:

Microalbuminaemia – slightly raised albumin A:CR 3-30mg/mmol

Treatment:

Intensive DM control
BP<130/80  use ACEi or ARB for CV and renal protection
Sodium restriction
Statins tp reduce CV risk

Question 61

Q

CKD

causes:

Rfx:

presentation:

Answer

A

CKD

Causes:

Diabetes
Hypertension
Age-related decline
Glomerulonephritis
Polycystic kidney disease
Medications like NSAIDs, PPIs and lithium

Risk factors for CKD

Older age
Hypertension
Diabetes
Smoking
Medications

Presentation

Often asymptomatic
Pruritis (itching)
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
Hypertension

Question 62

Q

investigations for CKD

complications

Answer

A

eGFR –> done via U&E test
proteinuria–> done via urine A:C
haemauria–> via urine dipsytick
renal USS

complications

Anaemia
Renal bone disease
CV
Peripheral neuropathy

Question 63

Q

ddx CKD

what investigation must be done before a renal biopsy

Answer

A

Differential diagnosis for CKD

Acute kidney injury
Alport syndrome
Antigiomerular basement membrane disease
Chronic glomerulonephritis
Diabetic nephropathy
Multiple myeloma
Nephrolithiasis
Nephrosclerosis
Rapidly progressive glomerulonephritis
Renal artery stenosis

Question 64

Q

Glomerulonephritis

Includes nephritic and nephrotic syndrome. What is the difference?

Answer

A

Term encompasses a number of conditions which:

Are caused BY pathology in the glomerulus
Present with proteinuria/+ haematuria
Are diagnosed with renal biopsy
Cause CKD
Can progress to renal failure

Nephrotic–> proteinuria from podocyte damage

Nephritic–>haematuria–> inflammation damage

Answer 62

A

Renal causes

Glomerulonephritis
IgA nephropathy
Polycystic kidney disease
Sickle cell disease
Haemophilia
Malignancy–> kidney,

Urinary tract

Malignancy–>ureter, bladder
Calculi (stone)
UTI

Answer 63

A

t4 –> T3

Answer 64

A

The clinical effect of excess thyroid hormone.

Much more common in women

Causes:

Grave’s disease–> IgG
Toxic multinodular goitre
Toxic adenoma
Ectopic thyroid tissue
Exogenous

Answer 65

A

(↓TSH /↑FT4 / ↑FT3)

causes

Grave’s disease
Toxic adenoma, Toxic MNG
Thyroiditis
Amioderone

Answer 66

A

↑TSH / ↑FT4 / ↑FT3)

TSHoma

Answer 67

A

Weight loss
Increased appetite
Anxiety/ nervousness
Sweating
Heat intolerance
Periorbital swelling
Goitre
Eye symptoms–> Grave’s disease
Frequent bowel movements
Thin skin/ brittle skin
Shorter lighter periods
Irritability
Coarse hair before losing it
Proptosis eye bulging

Answer 68

A

Tachycardia
Warm, moist skin, tremor, lid retraction (see whites of eyes above and below)
Goitre
Pretibial myxoedema swelling of lateral malleolus
Thyroid acropachy extreme presentation with nails lifting off of beds

Answer 69

A

↓TSH and TRH (supressed) due to negative feedback effect of T3 and T4)
Thyroid autoantibodies
Isotope scan
Test visual fields in ophthalmopathy

Answer 70

A

1) Drugs: B-blockers e.g., propranolol for rapid control of symptoms

Antithyroid medication

a) titration method- carbimazole/ (thiomide)–> reduce every 2 months and check TFTs
b) block and replace- carbimazole + levothyroxine

Carbimazole SE–> agranulocytosis

2) Radioiodine–> social restrictions while on medication. Be careful to administer during thyroid storm
3) Thyroidectomy (usually total)

risk of damage to recurrent laryngeal nerve  hoarse voice

also risk of causing hypothyroidism

Answer 71

A

Aim of ATDs is to bring people into remission and become euthyroid again. In this case the drugs can be discontinued.
High relapse rate after the first round of ATDs however

Answer 72

A

The clinical effect of a lack of thyroid hormone.

Causes:

a. Primary (↑TSH / ↓FT4 / ↓FT3)
* Goitre- Hashimoto’s thyroiditis (TPO antibodies

Iodine deficiency
Drugs (Amiodarone; Lithium- inhibits TSH; Iodine
Non-goitrous – post surgery
Atrophic thyroiditis

b. Central-** **(↓TSH / ↓FT4 / ↓FT3)

Pituitary–> isolated TSH deficiency; hypopituitarism

Hypothalamic

Answer 73

A

Symptoms:

Weight gain
Constipation
Fatigue
Brain fog
Depression
Goitre–> hoarse voice
Muscle aches
Dry coarse skin and hair loss
Hoarseness
Puffy face
Cold intolerance
Bradycardia
Longer heavier periods

Answer 74

A

Signs BRADYCARDIC

Bradycardic
Slow reflexes
Ataxia
Dry thin skin
Yawning/ drowsy
Cold hands
Round puffy face
Defeated demeanour
Immobile ileus
CCf

Answer 75

A

Levothyroxine (T4)

Amiodarone (iodine rich drug)

Answer 76

A

HYPOALDRENALISM opposite of cushing’s

Primary–> abnormality of the adrenal gland

Secondary–> disorder of the HPA axis (ACTH secretion)

effects of cortisol

Regulates glucose levels opposes insulin  increases blood c
Anti-inflammatory
Promotes breakdown of fat
Increase liver gluconeogenesis
Muscle decreases amino acid uptake by muscle
Reduces bone formation

Answer 77

A

Tumours – pituitary, craniopharyngioma, metastases
Infarction – pituitary stalk compression, Sheehan’s syndrome
Infections - TB
Inflammation – sarcoidosis, histocytosis X, haemochromatosis, lymphocytic
hypophysitis
Iatrogenic – surgery, radiotherapy, OVERUSE OF STEROIDS (very common cause)
Drugs – Opiates, Steroids*
Other – trauma, isolated ACTH deficiency

Answer 78

A

Usually, an autoimmune disease that results in PRIMARY ADRENAL INSUFFICIENCY via destruction of the adrenal cortex.

Can often be found amongst other autoimmune conditions  e.g., vitiligo

Affects adults 30-50 years

Answer 79

A

Risk factors

Have cancer
Anticoagulants
Chronic infections like TB
Adrenalectomy
Comorbid autoimmune disease t1dm or Graves’

Answer 80

A

• Autoimmune 70% AKA –> autoimmune adrenalisitis
• Infection – TB, Fungal, Opportunistic
• Infarction – Thrombosis in Anti-phospholipid syndrome
• Haemorrhage – Waterhouse-Friedrichsen syndrome
• Infiltration – Amyloidosis, Haemachromatosis
• Malignancy – Lung/Breast/Kidney metastasis; Lymphoma
• Iatrogenic – Adrenalectomy, ketoconanzole (and other anti-fungals)
- Drugs Ketoconazole / Fluconazole/Phenytoin / Rifampicin/ Steroids*

Phaeochromocytoma phaeo is an adrenal secreting tumour

Answer 81

A

Lethargy

Dizziness postural hypertension

Anorexia or weight loss

Hypoglycaemia

Nausea, vomiting, abdominal/ back pain, diarrhoea

Hyperpigmentation

Sun exposed areas, pressure areas

Scars, palmar erythema, oral mucosa

Answer 82

A

↓Na+ / ↑K+ (as a result of ↓in mineralocorticoids)
↑Urea
Mild ↑Ca2+
Anaemia (normocytic, normochromic unless B12 deficiency)

Answer 83

A

ACTH levels

synacthen test long or short

Answer 84

A

Glucocorticoid replacement therapy
- Hydrocortisone 10mg on waking
  - 5mg midday
  - 5mg evening (alternatively can be given twice daily)
Aim for lowest dose that allows patient to feel well
Doses should be doubled doubled during times of intercurrent illness
Patients should carry steroid card and shock pack of IM hydrocortisone
Mineralocorticoid therapy if primary insufficiency

Answer 85

A

Medical emergency- urgent treatment essential

Worsening of the general condition with signs and symptoms of glucocorticoid and or mineralocorticoid + worsening of:

clinical features

Shock/ hypotension
Oliguria
Weak
Confused
Nausea
Vomiting
Abdominal pain (think acute abdomen)
Fever
Hypoglycaemia

Answer 86

A

If suspected treat before lab results are back

Bloods–> cortisol, ACTH, U+E’s (¯Na+ K+)
Hydrocortisone 100mg stat IV
IV fluid bolus e.g., 500mL 0.9% saline
Monitor blood glucose to prevent hypoglycaemia

Answer 87

A

Adrenal gland cortexes produce 3 kinds hormone

Glucocorticoids–> cortisol–> carbohydrate, lipid and protein metabolism (G-glomerulosa)
Mineralocorticiods–> aldosterone–> sodium and potassium balance (F- fasiculata)
Androgens (R-reticularis)

Cushing’s syndrome- State caused by chronic glucocorticoid excess (exogenous or endogenous) + loss of normal negative feedback mechanisms to HPA axis + loss of circadian secretion of cortisol

Chief cause: steroid use

Answer 88

A

ACTH dependant - excessive ACTH from the pituitary gland e.g,. tumour (Cushing’s disease) or ectopic ACTH secretion in small cell lung cancer

ACTH independant- adrenal cortisol excess (adrenal tumours or adenomas) or exogenous steroids

Answer 89

A

Fatigue
Lethargy
Proximal muscle weakness
Peripheral oedema
Weight gain
Depression, mood swings, insomnia
Irregular periods
Reduced libido
Facial plethora (redness)
Buccal hyperpigmentation (black)
Headaches and visual field defects if pituitary adenoma

Answer 90

A

Thin skin–> easy bruising
Central obesity (potato on 2 sticks)
Buffalo hump
Purple striae (abdominal stretch marks)
Moon face
Hirustism (women gain facial hair)

differential diagnosis

hypothyroidism
depression
PCOS- polycystic ovary disease
T2DM

Answer 91

A

Overnight dexamethasone suppression test- AM cortisol should be low if normal health
24 hr urinary cortisol
Elevated late night salivary cortisol
None of these determine cause of hypercortisolaemia

Answer 92

A

Plasma ACTH

raised–> pituitary adenoma or ectopic ACTH secretion

low–> ACTH independent cause

High dose dexamethasone suppression test distinguishes between pituitary and ectopic ACTH secretion –> suppreses primary but not ectopic

Inferior petrosal sinus sampling - ACTH levels measured from veins draining pituitary gland and these are compared to peripheral ACTH levels

Scans for cushings

CT chest looking for ectopic ACTH

MRI adrenals

MRI pituitary

Answer 93

A

definitive treatment is surgical (trans-sphenoidal surgery, bilateral adrenalectomy)

medical (metyrapanone)

radiotherapy

Answer 94

A

Clinical features and biochemical evidence of cortisol excess–> but not caused by hypothalamic-pituitary axis.

Depression
Alcohol excess
Obesity

Complications of pseudocushings

Hypertension

Diabetes

Osteoporosis

Prone to infections

Answer 95

A

Low Hb level–> due to either low red cell mass or increased plasma volume (e.g., in pregnancy).

What is considered a low Hb level:

<135g/L for men

<115g/L for women

decreased RBC production or increased RBC destruction

Answer 96

A

Fatigue
Dyspnoea
Faintness
Palpitations
Headache
Tinnitus
Anorexia

Angina If pre-existing coronary artery disease

Answer 97

A

Microcytic anaemia- LOW MCV- TAILS

Thalassaemia- really low MCV despite raised RBC
Anaemia fo chronic disease
Lead poisoning
Iron deficiency anaemia- most common cause
Sideroblastic anaemia (very rare)

Normocytic anaemia- Normal MCV- AAAHH

Acute blood loss
Anaemia of chronic disease
Aplastic anaemia
Hemolysis
Hypothyroidism
Bone marrow failure
Renal failure
Pregnancy
Bone marrow failure- if low WCC or decreased platelet

High MCV (Macrocytic anaemia)

B12 or folate deficiency
Alcohol excess or liver disease
Reticulocytosis
Cytotoxins (hydroxycarbamide)
Myelodysplsatic syndromes–> go onto develop AML
Marrow infiltration
Hypothyroidism
Antifolate drugs

haemolysis

Answer 98

A

most common kind of anaemia

causes:

Blood loss (e.g., menorrhagia or GI bleeding)
Poor diet or poverty may cause in children
Malabsorption (e.g., coeliacs)
Hookworm in tropics
signs:
Koilnychia (spoon shaped nails)
Atrophic glossitis (bald swollen red tongue)
Angular cheilosis / AKA stomatitis ulceration at the side of the tongue

tests:

Blood film

Microcytic
Hypochromic
Poikilocytosis increase in abnormal RBC of any shape
Anisocytosis RBCs that are different sizes

Decreased ferritin

Coeliac serology

Stool microscopy if relevant travel history

Answer 99

A

ferrous sulfate

Answer 100

A

Acute- impaired cell differentiation, resulting in large numbers of malignant precursor cells in the. Bone marrow (blasts) –> CML, CLL

Chronic- Excessive proliferation of mature malignant cells, but cell differentiation is unaffected

Answer 101

A

Malignancy of lymphoid cells affecting B or T lymphocytes therefore uncontrolled proliferation of blast cells causing marrow failure and tissue infiltration
Commonest cancer of children- rare to see in adults

Answer 102

A

a) Bone marrow failure–> anaemia, infection (¯WCC) and bleeding (¯platelets)
b) infiltration–> hepato and splenomegaly, lymphadenopathy–> superficial (cervical, axillary, groin) or mediastinal, CNS involvement (cranial nerve palsies), orchidomegaly

tests:

FBC– neutropenia
Blood film– characteristic blast cells
CXR and CT scans: look for mediastinal and abdominal lymphadenopathy
Lumbar punctures– look for CNS involvement

Answer 103

A

Supportive:

- Blood/ platelet transfusion
- IV fluids
- allopurinol (prevents tumour lysis syndrome)
- Insert a subcutaneous port system/ Hickman Line for IV access

Infections:

- Immediate IV abx
- Start neutropenia regimen
- Give prophylactic antivirals, antifungals, Abx

Chemo:

Complex and multi drug regimen (more information in notes)
- Drugs include vincristine, prednisolone, L-asparaginase + daunorubicin

Match related marrow allogenic BM transplant:

When in remission (no evidence of blasts in blood and <5% blasts in marrow)

Answer 104

A

Rapid progression

Neoplastic proliferation of myeloid blast cells

Most common acute leukaemia in adults

Answer 105

A

Signs and symptoms of CML

a) Bone marrow failure- anaemia, infection (dec WCC/ neutropenia), bleeding, DIC
b) Infiltration-hepatomegaly, splenomegaly, gum hypertrophy, Skin involvement

diagnosis of CML

WCC but can be normal or even low
Bone marrow biopsy (few blast cells in the periphery) differentiated from ALL by presence of Auer rods (crystals of coalesced granules)

Answer 106

A

CML

Uncontrolled proliferation of myeloid cells
Occurs most often in 40-60 year olds
Presence of Philadedlphia chromosome in >80% Philadelphia chromosome (BCR-ABL gene fusion due to translocation of chromo 7 and 22)

Symptoms

Mostly chronic and insidious
¯weight
Tiredness
Sweats
Features of gout???
Bleeding bruising (thrombocytopaenia)
Abdominal discomfort from splenomegaly

Tests

Very high WBC with whole spectrum of myeloid cells
Low Hb or normal
High urate
B12 increase

Answer 107

A

what is the hallmark of this cancer?

progressive accumulation of incompetent B cells

symptoms

often none, often found as a surprise fiding on routine FBC
Anaemic
Infection prone
Decreased weight
Sweats
Anorexia

signs

Enlarged, rubbery, non-tender nodes (DDx: lymphoma)

tests

Increased number of lymphocytes
Blood film- Smudge cells (cells with lack of cytoskeletal protein)
later–> marrow infiltration, ¯Hb, ¯neutrophils and platelets

complications?

Autoimmune haemolysis
Increased infection especially herpes zoster

Answer 108

A

Obstruction (stricture) of the oesophagus- dysphagia
Pain- prevents eating
Difficult after surgery- eat smaller and more frequent meals, soft foods
General cachexia syndrome- increased metabolism, loss of skeletal muscle, fatigue and loss of appetite

Answer 109

A

Cancerous cells demand more energy than normal cells- metabolic rate is higher than normal.
Cytokines against tumours interfere with hormones that control appetite
Nausea from cancer and chemotherapeutic drugs prevent eating.
Cancers nearby in the abdomen such as ovarian cancer can press on the stomach - mass effect.
Mental and emotional effects of cancer take their toll to decrease appetite- stress, anxiety

Answer 110

A

Causes of malabsorption Common

Coeliac disease
Chronic pancreatitis
Crohn’s disease

Causes of malabsorption Rare

¯Bile: primary cholangitis, ileal resection, biliary obstruction

Pancreatic insufficiency: pancreatic cancer, cystic fibrosis

Drugs: metformin, alcohol

Small bowel: small bowel resection

Bacterial overgrowth

Infection

Answer 111

A

Symptoms:

Diarrhoea
¯Weight
Lethargy
Steatorrhea
Bloating

Resultant deficiency signs

Anaemia Fe, B12, folate
Bleeding disorders  K+
Metabolic bone disease vit D

Answer 112

A

Suspect this if:

Diarrhoea, weight loss or anaemia (esp. if iron or B12 is low)

Associated with: autoimmune disease  dermatitis herpetiformis

Peak ages of incidence diagnosis–> childhood and 50-60

6x chance in 1^st degree relatives

Answer 113

A

Presentation

Stinking stools/ steatorrhea
Diarrhoea
Abdominal pain
Bloating
Nausea and vomiting
Apthous ulcers (oral)

Non GI

ANAEMIA
Weight
Fatigue
Osteomalacia (soft bones)
Infertilitiy
Failure to thrive
Angular stomatitis

Answer 114

A

Hb (<130 in men, <120 in women)
¯ B12, Ferritin
Antibodies–> anti-transglutaminase
Duodenal biopsy (villous atrophy, inter-villous WBCs, crypt hyperplasia)

Answer 115

A

Chronic inflammatory disease characterised by transmural granulomatous affecting any part of the GI tract from the gut to the mouth especially the terminal ileum.
Skip lesions (intermittent areas unaffected) unlike UC

Typically presents at what age? 20- 40 (peak 30 with second peak at 50

Answer 116

A

Symptoms:

Diarrhoea
Abdominal pain
Weight loss
Fatigue
Fever
Malaise

Signs

Bowel ulceration
Abdominal tenderness
Perianal fistula/ skin tags/ anal strictures

Answer 117

A

Complications

Small bowel obstruction
Abscess formation
Fistulae (e.g., colo-vaginal)
Malnutrition –> makes your bowel leaky –> lack enough protein to make albumin
Perforation

Answer 118

A

Tests

Colonoscopy and biopsy
Stool: CDT–> c.difficile toxin, faecal calprotectin
Bloods: FBC, ESR, CRP, U & E, LFT, INR, ferritin, B12, Folate
Small bowel endoscopy
MRI–> assess pelvic disease + fistula, small bowel disease activity, strictures.
Abdo xray–> megacolon

Treatment

Reassurance and use of humour –> “no sex… no hope… no intimacy” dispel
Patients should be offered monotherapy with glucocorticoids (prednisolone or IV hydrocortisone).
Enteral nutrition may be considered as an alternative in children (as steroids suppress growth).
Azathioprine or mercaptopurine may be added on to induce remission if there are 2 or more exacerbations in a 12-month period or the glucocorticoid cannot be tapered
Biologics- anti-TNF, infliximab
Surgery
Severe admit for IV hydration/ electrolyte replacement, IV steroids, consider need for blood transfusion

Answer 119

A

Fat
Fluid
Foetus
Flipping big mass
Flatulence
Faeces

Answer 120

A

fresh frozen plasma

blood donor- O-

blood recipient AB+

plasma donor AB

plasma recipient O

Answer 121

A

Hodkins disease
Recipients of autologous stem cell transplants
Allogenic stem cell transplant
Congenital immunodeficiencies: SCID

Answer 122

A

fever
• chills
• rigors
• myalgia
• nausea
• mouth or throat
tingling or swelling
(angioedema)

• signs of anaphylaxis
• severe anxiety or sense of
impending doom
• skin rashes or itch

Answer 123

A

Agitation
Fever rapid onset
Hypotension
Flushing
Chest pain
TRALI (transfusion related acute lung injury)
Dyspnoea
Cough
White out

Answer 124

A

hypoalbuminaemia–> oedema

acute malnutrition

Kwashiorkor- protein deficiency
Bilateral pitting oedema
Distended abdomen
Hair thinning
Skin/ hair depigmentation
Dermatitis

Answer 125

A

Primary hyperaldosteronism

What kind of hormone is Aldosterone?

Mineralocorticoid steroid

Action of aldosterone?

Increases Na+ reabsorption - hypernatraemia
Increases K+ secretion - hypokalaemia
Increase hydrogen secretion - metabolic alkalosis

What is the name for primary hyperaldosteronism? - conn’s syndrome

When the adrenal gland are directly responsible for producing too much aldosterone

Serum renin ↓ : serum aldosterone ↑

Answer 126

A

Causes for primary hyperaldosteronism

Adrenal adenoma (benign)
Bilateral adrenal hyplasia
Familial hyperaldosteronism
Adrenal carcinoma

Secondary hyperaldosteronism

Excessive renin stimulates the adrenal glands to produce more aldosterone

Serum renin will be high

Serum renin ↑ : serum aldosterone ↑

Causes of secondary hyperaldosteronism

BP in kidneys> resot of body
Renal artery stenosis (narrowing of artery atherosclerotic plaque, confirm with doppler ultrasound, CT angiogram or magnetic resonance angiography)
Renal artery obstruction
Heart failure

Answer 127

A

Hypokalaemia- <3.5mmol/L
- Sm. Muscle
  - Constipation
- Sk. Muscle
  - Weakness
  - Cramp
  - Flaccid paralysis
- Respiratory muscle
  - Resp depression
- Cardiac muscle
  - Arrhythmias
- Fatigue
Hypernatraemia >140 mmol/L

Excessive thirst

Hypertension

Dizziness
Blurred vision

Headaches

Polyuria

Metabolic alkalosis

Answer 128

A

Screen the chronically hypertensive via renin : aldosterone blood sample
BP-hypertension
U & E’s - hypokalemia + hypernatraemia
ABG- alkalosis
ECG- prolonged QT, U waves present, atrial + vent tachycardia
Suppression test (saline or captopril)
24 hr urinary excretion of aldosterone test
CT/ MRI - look for adrenal tumour
Renal doppler ultrasound/ CT angio/ MRA  look for renal stenosis or obstruction
Adrenal vein sampling- compare aldosterone from each gland

Answer 129

A

Coarctation of the aorta
Fibromuscular dysplasia
Congestive heart failure
Nephrotic syndrome
Diuretic use

management

Treat underlying cause
- Tumour- surgical removal via laparoscope
- Renal artery stenosis- percutaneous renal artery angioplasty
Aldosterone antagonists
- Spironolactone- non-selective antagonist  also blocks testosterone receptors gynecomastia, menstrual problems, erectile dysfunction
- Eplerenone- new selective aldosterone antagonist ?less side effects
Lifestyle factors
- Low salt diet
- Smoking cessation
- Limit alcohol intake
- Exercise regularly

Answer 130

A

140/90 in adults and 150/90 in the elderly

Renal disease:

Most common cause 75%
Intrinsic renal disease: glomerulonephritis, chronic pyelonephritis
Endocrine: Cushing’s, conn’s, phaeochromocytoma (tumour that secretes too much adrenaline), acromegaly, hyperparathyroidism
Others: coarctation, pregnancy
drugs: MAOIs, steroids, oral contraceptive pills, cocaine, amphetamines

Answer 131

A

Supply/demand imbalance of nutrients, energy required for growth, maintenance and function.

Difference between kwashiorkor and marasmus:

a. kwashiorkor- inadequate protein intake with adequate total caloric intake

b. marasmus- inadequate protein, caloric intake

malnutrition link to immune function

impairs immune function - increase likelihood of infection – increase nutritional demand — further malnutrition

chance of refeeding syndrome

Answer 132

A

Due to secretion of growth hormone from a pituitary tumour or hyperplasia (e.g,. via ectopic GH releasing from a carcinoid tumour).

GH stimulates growth of bone and soft tissue through secretion of IGF-1.

symptoms

Acroparathesia (tingling in the extremities acro means extremities)
Amenorrhoea
↓libido
Headache
Sweating
Snoring
Arthralgia
Backache
Wonky bite
Curly hair

Answer 133

A

signs of acromegaly

Growth of hand size (spade like)
Jaw and feet growth
Wide nose
Big supraorbital ridges
Macroglossia
Widely spaced teeth
Skin darkening
Obstructive sleep apnoea
Goitre
Hemianopia mass effect of pituitary tumour

Answer 134

A

complications

Diabetes
Left ventricular hypertrophy  CHF
Ischaemic heart disease

Tests for

Hyperglycaemia
Hypercalcaemia
Increased phosphate

Diagnosis for acromegaly

IGF-1 measurement- after you’ve fasted overnight (normally GH inhibited by glucose so you need to eliminate it from the system as much as possible)
Growth hormone suppression test- before and after glucose drink

Answer 135

A

Excise lesion- tans sphenoidal surgery (1^st line)  (2^nd) somatostatin analogue- radiotherapy

2 conditions that can cause abdominal pain

IBD
Peptic ulcer

Name 2 diseases that can cause loose stools:

crohns, coeliacs, lactose intolerance

Answer 136

A

a) Gastrointestinal

Gastroenteritis
Peptic ulceration
Pyloric stenosis
Intestinal obstruction
Paralytic ileus
Acute cholecystitis
Acute pancreatitis

b) CNS

meningitis/ encephalitis

migraine
raised intracranial pressure
motion sickness
labrynthitis

c) Metabolic/ endocrine

uraemia
hypercalcaemia
hyponatraemia
pregnancy
DKA
Addison’s disease

d) alcohol and drugs

antibiotics
opiates
cytotoxins
digoxin

Sepsis

Answer 137

A

Unpredictable disease w mortality of 12%

Characterized by self-perpetuating pancreatic autodigestion, oedema and fluid shifts cause hypovolaemia.

80% mild cases 20% develop severe complications

Answer 138

A

all stones (~35%)
thanol (~35%)
rauma
teroids
umps
utoimmune
corpion venom
yperlipidaemia, hypothermia, hypercalcaemia
RCP and emboli
rugs

Answer 139

A

Gradual or sudden epigastric or central pain (radiates to back and eased when leaning forwards). Vomiting prominent

signs of pancreatitis

May be subtle even in severe disease
↑HR
Fever
Jaundice
Shock
Ileus
Rigid abdomen
Periumbilical bruising (Cullen’s sign)
Bruising on flanks (Grey Turner’s sign)

Answer 140

A

Raised serum lipase
Raised serum amylase
CRP
CT gold standard
US look for gallstones

management

Modified Glasgow criteria is crucial for assessing severity
Nil by mouth - consider NJ feeding
Crystalloid IV to combat third spacing
Urinary catheter
Analgesia- pethidine
ERCP for progressing gallstone severity

Answer 141

A

Barium meal is a diagnostic test used to detect abnormalities pf the oesophagus, stomach and small bowel using x ray images

Answer 142

A

1) Malabsorption- Malnutrition

Coeliacs
IBD
Chronic pancreatitis

2) Endocrine

Diabetes mellitus (1 and 2)
Hyperthyroidism
Hypoadrenalism

3) Renal

CKD

4) Cancers

ESPECIALLY gi
5) Mental health conditions
Depression
Anxiety
Eating disorders
OCD

Answer 143

A

Endocrine

Hypothyroidism

Cushing’s Syndrome

AKI

Too much grehlin (stimulate appetite and promote fat storage)

Too little cholecystokinin (stimulates pancreas to release enzymes and communicates fullness)

Oedema –cirrhosis, nephrotic syndrome, heart failure

Medication – antipsychotics

Acromegaly

Answer 144

A

Goitre- hyper/ hypothyroidism
Lymphadenopathy- infective (TB, EBV, HIV), sarcoidosis, amyloidosis, Rheumatoid, Chronic Lymphyocyte Leukaemia

Tiredness makes you think of:

Cushing’s Syndrome

Anaemia

Hypothyroidism

Answer 145

A

T2DM
Coronary heart disease
some types of cancer
stroke
heartburn
sleep apnoea
osteoarthritis
COVID-19 symptoms
hypertension
dyslipidaemia
gallbladder disease

Answer 146

A

thrombocytopaenia

Answer 147

A

Shock- circulatory failure resulting in organ hypoperfusion. SBP < 90mmHg or MAP < 65mmHg with evidence of hypoperfusion (mottled skin, high lactate (>2mmol/l), urine output <0.5 mmol/L)

signs of shock

↓GCS
agitation
pallor
cool peripheries
tachycardia
slow cap refill
tachypnoea
oliguria

Answer 148

A

If suspected treat before biochemical results

Bloods cortisol and ACTH… U & E ↑K (trat with calcium gluconate) + ↓Na (rehydration and steroids)

Hydrocortisone 100mg IV stat

IV fluid bolus 500mL 0.9% saline

Monitor blood glucose  look for hypoglycaemia

Monitor shock  lactate

Answer 149

A

Pulses (strong or weak)
Cap refill time in fingers or sternum
Resp rate tachypnoea think peripheral oedema
Auscultate lungs listen for coarse crackles
Abdominal distension in overload
Shifting dullness
Striae (stretch marks) in hypervolaemia
Sacral oedema
Pitting oedema
Look at mucous membranes  e.g., eyes and tongue

Answer 150

A

lactic shock (shock, infection, tissue ischaemia)
urate (renal failure)
ketones (diabetes mellitus, alcohol)
drugs/ toxins (salicytes, methanol)

Answer 151

A

Vomiting

K+ depletion

Burns

Ingestion of base

Answer 152

A

Type 2 respiratory failure- 02 low - usually COPD- use venturi mask

↑pH ↓CO2

Almost always due to hyperventilation of any cause stroke, subarachnoid bleed, meningitis

Answer 153

A

presentation

lethargy
Thirst
weakness
Irritability
Confusion coma
Signs of dehydration

causes

Usually due to water loss on excess of Na+ loss
Fluid loss without replacement (burns, diarrhoea, vomiting)
Diabetes insipidus
Diabetes mellitus
Primary aldosteronism (Addison’s)

Answer 154

A

anorexia
nausea
headache
irritability
confusion
weakness

Answer 155

A

Presentation

Fast irregular heartbeat
Angina
Lightheadedness
ECG changes tall tented/hyper acute T waves, small p waves, wide QRS complex and eventual ventricular fibrillation

Causes of hyperkalaemia

Oliguric renal failure
K+ sparing diuretics
Rhabdomyolysis
Metabolic acidosis
Excess K+ therapy
Addisons disease
Massive blood transfusion
Burns
Drugs ACE-i

Answer 156

A

If K+ >2.5mmol/L

Hypokalaemia perpetuates digoxin toxicity

Signs and symptoms

Hyporeflexia

Hypotonia

Muscle weakness

Cramps

Constipation

ECG changes small or inverted T waves, long PR interval, depressed ST segments

Vomiting and diarrhoea

Pyloric stenosis

Cushings syndrome/ steroids/ ACTH

Conn’s syndrome (hypoaldosteronism)

Alkalosis

Renal tubule failure

Answer 157

A

overnight dexamethosone suppression test.

dexamethosone is a steroid like cortisol. by increasing serum steroid, you see if the pituitary gland stops secreting acth.