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Year 3 Med 2 > Med 2 LOs > Flashcards

Med 2 LOs Flashcards

1
Q

risk factors for peptic ulcer disease

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
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2
Q

Symptoms of peptic ulcer disease

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

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3
Q

differential diagnosis peptic ulcer

A

GORD

gastritis

oesophageal varicoeal bleed

sleep apnoea

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4
Q

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

A

gastroduodenal artery

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5
Q

investigations for peptic ulcer disease

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
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6
Q

management of peptic ulcer disease

A
  1. ABC approach as with any upper gastrointestinal hemorrhage
  2. First line treatment is endoscopic intervention
  3. Stopped medication contributing to dyspepsia
  4. Interventional angiography with transarterial embolization or surgery
  5. If H. pylori +ve - 1 IV proton pump inhibitor (osemoprazole, lansoprazole) + 2 Antibiotics (amoxicillin, clarithromycin, metronidazole, tetracycline)
  6. If H.Pylori -ve –> acid suppression alone
  7. If intolerant to PPI try H2RA- ranitidine
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7
Q
  • Outline the fluid management of a patient with a GI haemorrhage.
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

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8
Q

differential diagnosis for someone with GI bleeding

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
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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

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

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10
Q

how would you rescuscitate someone after an upepr GI bleed?

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
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11
Q

ways of treating an upper GI bleed with an endoscope

  1. non-variceal bleed
  2. variceal bleed
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

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12
Q

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

A
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13
Q

Physiology of vomiting

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
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14
Q
A
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15
Q

differential diagnosis for. aptient with a change in bowel habit

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
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16
Q

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

A

Prothrombin time (PT)

APTT

INR

FBC

Albumin

D/dimer

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17
Q

what is prothrombin time

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
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18
Q

what is APTT

what diseases are likely to cause a change in it?

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)
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19
Q

What is INR

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).

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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
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
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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?
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
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22
Q

Haemophilia A

A

Factor 8 deficiency

80% of haemophilias

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

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23
Q

Haemophilia B (Christmas disease)

A

factor 9 deficiency

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24
Q

Signs and symptoms for haemophilia

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
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25
Q

diagnosis of the haemophilias

treatment

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

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26
Q

vitamin K deficiency

which vitamins are fat soluble

causes of K deficiency

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​
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27
Q

symptoms of vitamin K deficiency

treatment

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

phytonadione

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28
Q

Von Willebrand disease

what does vWf do?

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
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29
Q

vWillebrand disease

symptoms

diagnosis

which antibiotic can cause it

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

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30
Q

Form a differential diagnosis for someone presenting with tiredness

<1 month

chronic

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
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31
Q

diabetes

which population is type 1 more frequent in?

complications of both types of diabetes?

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
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32
Q

diagnosis of DM

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
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33
Q

alternative causes for hyperglycaemia

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

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34
Q

T1DM

AKA?

what % of DM cases?

patho?

epidemiolgy?

associated with what?

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
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35
Q

symptoms of T1DM?

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
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36
Q

treatment of T1DM

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
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37
Q

T2DM

what % of DM cases?

patho?

linked to what?

acquired or inherited?

causes (2)

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
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38
Q

symptoms of T2DM

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

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39
Q

risk factors for T2DM

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)
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40
Q

treatment for T2DM

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 1st line- reduces hepatic gluconeogenesis, increase skeletal muscle glucose uptake –> contraindicated in renal problems
  • Sulfonylureas 2nd line – gliclazide, glipizide, insulin secretagogue
  • Thiazolidinediones 3rd line – pioglitazone
  • Alpha-glucosidase inhibitors- acarbose
  • GLP-1 receptor analogues
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41
Q
A
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42
Q

how does renal disease present? (2)

A
  1. asymptomatically
  2. renal tract symptoms
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43
Q

how do you detect renal disease in

  1. asymptomatic presentation
  2. renal tract symptoms
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
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44
Q

Acute renal disease (AKI)

what is it? how is it measured?

definition by diagnosis?

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
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45
Q

how do you stage an AKI?

risk factors for an AKI

A

serum creatinine vs urine output

  • Pre-existing CKD
  • Age
  • Male
  • Comorbidity (DM, cardiovascular disease, malignancy, chronic liver disease, complex surgery)
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46
Q

symptoms of an AKI

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
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47
Q

causes of an AKI

A
  1. Sepsis
  2. Major surgery
  3. Cardiogenic shock
  4. Other hypovolaemia
  5. Drugs
  6. Hepatorenal syndrome
  7. Obstruction
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48
Q

aetiology of an AKI can be split into 3:

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

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49
Q

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

A

Nephritic

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50
Q

Differential diagnoses of an AKI

A
  • Chronic kidney disease
  • Hypoglycaemia DM
  • Renal calculi
  • Sickle cell anaemia
  • Dehydration
  • GI bleed
  • Heart failure
  • UTI
  • Protein overload
  • DKA
  • Urinary obstruction
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51
Q

Investigations of AKI

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
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52
Q

U&Es for kidney injuries/ dysfunction

A

High potassium, high creatinine and high urea

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53
Q

what are 2 examples of acute renal diseases?

A

Nephrotic syndrome

Diabetic Nephropathy

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54
Q

nephrotic syndrome

triad of:

commonest cause in young people?

A

presents with the classic triad of:

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

may also see hypercoagulability

Commonest cause in a young person–> autoimmune

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55
Q

Aetiology of nephrotic syndrome

primary renal and secodnary to systemic

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
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56
Q

presentation of nephrotic syndrome

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
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57
Q

investigations for nephrotic syndrome

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

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58
Q

management of nephrotic syndrome

A
  1. 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
  2. Treat underlying cause
    1. Renal biopsy
    2. Steroids
  3. Reduce proteinuria
    1. ACE-i/ ARB reduces proteinuria
  4. Manage complications–> e.g., give anticoagulants
  5. Immunosuppression –> for causes like lupus???
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59
Q

complications of nephrotic syndrome

A
  1. Malnutrition–> nephrotic for a long time
  2. Thromboembolism
  3. Infection (urine losses of immunoglobulins)
  4. Hyperlidipaemia –> increased cholesterol + ↑triglyceridemic
  5. AKI/ CKI Renal failure → hyperkalaemia
  6. Hypertension
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60
Q

diabetic nephropathy

commonest cause of end stage renal failure

diagnosis:

treatment:

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
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61
Q

CKD

causes:

Rfx:

presentation:

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
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62
Q

investigations for CKD

complications

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
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63
Q

ddx CKD

what investigation must be done before a renal biopsy

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
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64
Q

Glomerulonephritis

Includes nephritic and nephrotic syndrome. What is the difference?

A

Term encompasses a number of conditions which:

  1. Are caused BY pathology in the glomerulus
  2. Present with proteinuria/+ haematuria
  3. Are diagnosed with renal biopsy
  4. Cause CKD
  5. Can progress to renal failure

Nephrotic–> proteinuria from podocyte damage

Nephritic–>haematuria–> inflammation damage

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65
Q

haematuria ddx:

A

Renal causes

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

Urinary tract

  • Malignancy–>ureter, bladder
  • Calculi (stone)
  • UTI
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66
Q

Hypothalamic-pituitary-adrenal axis

Out of T3 and T4, which in converted into which?

A

t4 –> T3

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67
Q

What is thyroxicosis

who is it much more common in

causes

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
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68
Q

hyperthyroidism effect on TSH FT4 and FT3

causes

A

(↓TSH /↑­FT4 / ­↑FT3)

causes

  • Grave’s disease
  • Toxic adenoma, Toxic MNG
  • Thyroiditis
  • Amioderone
69
Q

pituitary stimulation effect on TSH FT4 and FT3

causes

A

↑TSH / ­ ↑FT4 / ­↑FT3)

  • TSHoma
70
Q

Excessive Exogneous Thyroid hormones (¯TSH / ¯ FT4 / ­FT3)

Amiodarone excess

A
71
Q

Symptoms of hyperthryoidism

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
72
Q

signs of hyperthyroidism

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
73
Q

tests for hyperthyroidism

A
  • ↓TSH and TRH (supressed) due to negative feedback effect of T3 and T4)
  • Thyroid autoantibodies
  • Isotope scan
  • Test visual fields in ophthalmopathy
74
Q

treatments for hyperthyroidism

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

75
Q

complications of anti thyroid drugs

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
76
Q

Hypothyroidism (myxoedema)

causes

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

77
Q

Symptoms of hypothyroidism

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
78
Q

signs of hypothyroidism

A

Signs BRADYCARDIC

  • Bradycardic
  • Slow reflexes
  • Ataxia
  • Dry thin skin
  • Yawning/ drowsy
  • Cold hands
  • Round puffy face
  • Defeated demeanour
  • Immobile ileus
  • CCf
79
Q

treatment of hypothyroidism

A

Levothyroxine (T4)

Amiodarone (iodine rich drug)

80
Q

what is adrenal insufficiency

what are the effects of cortisol

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
81
Q

causes of secondary adrenal insufficiency

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
82
Q

Addison’s disease

what is it and who does it affect

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

83
Q

risk factors for addisons

A

Risk factors

  • Have cancer
  • Anticoagulants
  • Chronic infections like TB
  • Adrenalectomy
  • Comorbid autoimmune disease t1dm or Graves’
84
Q

causes of primary hypoaddrenalism

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

85
Q

Clinical features of primary hypoadrenalism/ Addison’s disease

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

86
Q

lab tests for addisons

A
  • ↓Na+ / ­ ↑K+ (as a result of ↓in mineralocorticoids)
  • ­ ↑Urea
  • Mild ­ ↑Ca2+
  • Anaemia (normocytic, normochromic unless B12 deficiency)
87
Q

adrenal insufficiency diagnosis

A

ACTH levels

synacthen test long or short

88
Q

treatment for adrenal insufficiency

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
89
Q
A
90
Q
A
91
Q

Addisonian crisis / acute adrenal crisis

clinical features

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
92
Q

Management of an addisonian crisis

A

If suspected treat before lab results are back

  1. Bloods–> cortisol, ACTH, U+E’s (¯Na+ ­K+)
  2. Hydrocortisone 100mg stat IV
  3. IV fluid bolus e.g., 500mL 0.9% saline
  4. Monitor blood glucose to prevent hypoglycaemia
93
Q

Cushing’s–> adrenal excess

the adrenal gland produces 3 kinds of hormone:

what is cushings syndrome and what is the chief cause

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

94
Q

2 classifications of Cushing’s cause

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

95
Q

symptoms of adrenal excess// cushings

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
96
Q

Clinical signs of Cushing’s

differential diagnosis

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
97
Q

how to confirm cushings syndrome

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
98
Q
A
99
Q

How to identify cause of cushings syndrome

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

100
Q

management of cushings

A

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

medical (metyrapanone)

radiotherapy

101
Q

psuedocushings

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

102
Q

what is anaemia

diagnostic amount

why may Hb be low?

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

103
Q

symptoms of anaemia

A
  • Fatigue
  • Dyspnoea
  • Faintness
  • Palpitations
  • Headache
  • Tinnitus
  • Anorexia

Angina If pre-existing coronary artery disease

104
Q

anaemias can be grouped into 3 by their relative size MCV

what are the causes of each

A

Microcytic anaemia- LOW MCV- TAILS

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

Normocytic anaemia- Normal MCV- AAAHH

  1. Acute blood loss
  2. Anaemia of chronic disease
  3. Aplastic anaemia
  4. Hemolysis
  5. Hypothyroidism
  6. Bone marrow failure
  7. Renal failure
  8. Pregnancy
  9. Bone marrow failure- if low WCC or decreased platelet

High MCV (Macrocytic anaemia)

  1. B12 or folate deficiency
  2. Alcohol excess or liver disease
  3. Reticulocytosis
  4. Cytotoxins (hydroxycarbamide)
  5. Myelodysplsatic syndromes–> go onto develop AML
  6. Marrow infiltration
  7. Hypothyroidism
  8. Antifolate drugs

haemolysis

105
Q

iron deficiency anaemia

causes

signs tests

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

106
Q

treatment for iron deficiency anaemia

A

ferrous sulfate

107
Q
A
108
Q

what is the difference between acute and chronic leukaemia

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

109
Q

Acute lymphoblastic leukaemia

which mature cells are affected

more common in kids or adults?

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
110
Q

Signs and symptoms of ALL

tests for ALL

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
111
Q

treatment for ALL

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)

112
Q

Acute myeloid leukaemia

how fast is progression?

kids or adults?

A

Rapid progression

Neoplastic proliferation of myeloid blast cells

Most common acute leukaemia in adults

113
Q

Signs and symptoms of CML

diagnosis of CML

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)
114
Q
A
115
Q

CML

  • occurs most frequenlty in which groups
  • presence of which chromosome in >80%
  • symptoms
  • tests
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
116
Q

CLL

what is the hallmark of this cancer?

symptoms

signs

tests

complications?

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
117
Q

how does carcinoma of the oesophagus cause weight loss?

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
118
Q

Why does cancer lead to weight loss

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
119
Q

causes of malabsoprtion (context: understand how malabsoprtion can lead to weight loss)

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

120
Q

symptoms of malabsorption disorders

A

Symptoms:

  • Diarrhoea
  • ¯Weight
  • Lethargy
  • Steatorrhea
  • Bloating

Resultant deficiency signs

  • Anaemia Fe, B12, folate
  • Bleeding disorders  K+
  • Metabolic bone disease vit D
121
Q

when should you suspect coeliacs?

coeliacs is associated with?

coeliac disease has a 6x higher chance in?

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 1st degree relatives

122
Q

presentation of coeliacs

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
123
Q

how is coeliacs diagnosed?

A
  • Hb (<130 in men, <120 in women)
  • ¯ B12, Ferritin
  • Antibodies–> anti-transglutaminase
  • Duodenal biopsy (villous atrophy, ­inter-villous WBCs, crypt hyperplasia)
124
Q
A
125
Q

ulcerative colitis and crohn’s disease comparison

  • location of inflammation
  • pattern of inflammation
  • appearance of inflammation
  • location of pain
  • bleeding
A

126
Q

Crohn’s disease

  • how many layers does granulation affect?
  • how far up the gI tract does crohns affect?
  • is this inflammation continuous?

epidemiology

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

127
Q

symptoms and signs of crohn’s disease

A

Symptoms:

  • Diarrhoea
  • Abdominal pain
  • Weight loss
  • Fatigue
  • Fever
  • Malaise

Signs

  • Bowel ulceration
  • Abdominal tenderness
  • Perianal fistula/ skin tags/ anal strictures
128
Q

Complications and tests for Crohns

A

Complications

  • Small bowel obstruction
  • Abscess formation
  • Fistulae (e.g., colo-vaginal)
  • Malnutrition –> makes your bowel leaky –> lack enough protein to make albumin
  • Perforation
129
Q

tests and treatment for Crohn’s

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
130
Q

what are the 6 F’s of abdominal swelling?

A
  • Fat
  • Fluid
  • Foetus
  • Flipping big mass
  • Flatulence
  • Faeces
131
Q

What blood product is used to correct clotting disorder?

which group is the universal:

blood donor?

blood recipient?

plasma donor?

plasma recipient?

A

fresh frozen plasma

blood donor- O-

blood recipient AB+

plasma donor AB

plasma recipient O

132
Q

who requires irradiated blood?

A
  • Hodkins disease
  • Recipients of autologous stem cell transplants
  • Allogenic stem cell transplant
  • Congenital immunodeficiencies: SCID
133
Q

symptoms of transfusion reaction

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

134
Q

symptoms of acute haemolytic reaction

A
  • Agitation
  • Fever rapid onset
  • Hypotension
  • Flushing
  • Chest pain
  • TRALI (transfusion related acute lung injury)
  • Dyspnoea
  • Cough
  • White out
135
Q

nephrotic syndrome effect on electrolyte and water balance

effects of acute malnutrition

A

hypoalbuminaemia–> oedema

acute malnutrition

  • Kwashiorkor- protein deficiency
  • Bilateral pitting oedema
  • Distended abdomen
  • Hair thinning
  • Skin/ hair depigmentation
  • Dermatitis
136
Q

what is conn’s syndrome

What kind of hormone is Aldosterone?

Action of aldosterone?

What is the name for primary hyperaldosteronism?

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 ↑
137
Q

Causes for primary hyperaldosteronism/ Conn’s

what is Secondary hyperaldosteronism

Causes of secondary hyperaldosteronism

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
138
Q

Signs and symptoms

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

139
Q

investigations for hyperaldosteronism

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
140
Q

DDx of hyperaldosteronism

management of primary and secondary

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
141
Q

what is considered to be hypertensive

what are secondary causes of hypertension

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
142
Q
  • what is malnutrition
  • what is the difference between kwashiorkor and marasmus
  • what is the link between malnutrition and immune function
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

143
Q

acromegaly

  • cause
  • patholhysiology
  • symptoms
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
144
Q

signs of acromegaly

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
145
Q

complications of acromegaly

tests for

diagnosis

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
146
Q

treatment for acromegaly

name 2 conditions that can cause abdominal pain

name 2 diseases that can cause loose stools

A

Excise lesion- tans sphenoidal surgery (1st line)  (2nd) 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

147
Q

DDX causes of vomiting

  • GI
  • CNS
  • Metabolic
  • Alcohol and drugs
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

148
Q

Acute pancreatitis

characterised by what

what percentage is mild vs severe

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

149
Q

causes of acute pancreatitis

get smashed

A
  1. all stones (~35%)
  2. thanol (~35%)
  3. rauma
  4. teroids
  5. umps
  6. utoimmune
  7. corpion venom
  8. yperlipidaemia, hypothermia, hypercalcaemia
  9. RCP and emboli
  10. rugs
150
Q

symptoms of acute pancreatitis

Signs of acute pancreatitis

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)
151
Q

tests for acute pancreatitis

management

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
152
Q

what is a Ba meal used for?

A

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

153
Q

DDx causes of weight loss

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
154
Q

differential diagnoses for cause of weight gain

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

155
Q

a lump in the neck makes you think of:

tiredness makes you think of:

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

156
Q

what are the health risks associated with weight gain?

A
  • T2DM
  • Coronary heart disease
  • some types of cancer
  • stroke
  • heartburn
  • sleep apnoea
  • osteoarthritis
  • COVID-19 symptoms
  • hypertension
  • dyslipidaemia
  • gallbladder disease
157
Q

gravitational petechial rash makes you think of

A

thrombocytopaenia

158
Q

definition of shock

signs of shock

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
159
Q

Management of shock from Addisonian crisis

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

160
Q

fluid assessment

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
161
Q

Metabolic acidosis causes: ↓pH ↓HCO3

A
  • lactic shock (shock, infection, tissue ischaemia)
  • urate (renal failure)
  • ketones (diabetes mellitus, alcohol)
  • drugs/ toxins (salicytes, methanol)
162
Q

causes for metabolic alkalosis ↑pH ↑HCO3-

A

Vomiting

K+ depletion

Burns

Ingestion of base

163
Q

resp acidosis

resp alkalosis

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

164
Q

hypernatraemia presentation and causes

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)
165
Q

hyponatraemia

presentation

A
  • anorexia
  • nausea
  • headache
  • irritability
  • confusion
  • weakness
166
Q

hyperkalaemia presentation and causes

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
167
Q

hypokalaemia

signs and symptoms

causes

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

168
Q

what is the first line initial bets test for diagnosing Cushing’s

A

overnight dexamethosone suppression test.

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

Year 3 Med 2 (9 decks)

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