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
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
3
Q
differential diagnosis peptic ulcer
A
GORD
gastritis
oesophageal varicoeal bleed
sleep apnoea
4
Q
which artery is most likely to be eroded in peptic ulcer disease
A
gastroduodenal artery
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
6
Q
management of peptic ulcer disease
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
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
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
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
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
11
Q
ways of treating an upper GI bleed with an endoscope
- non-variceal bleed
- 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
12
Q
by quadrant or area of the abdomen list what could cause pain
A
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
14
Q
A
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
16
Q
Which blood results can be used to interpret the coagulability of blood
A
Prothrombin time (PT)
APTT
INR
FBC
Albumin
D/dimer
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
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)
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).
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
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
22
Q
Haemophilia A
A
Factor 8 deficiency
80% of haemophilias
Levels may also be lower in von Willenbrand disease -look also at that
23
Q
Haemophilia B (Christmas disease)
A
factor 9 deficiency
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
25
diagnosis of the haemophilias
treatment
* 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
26
vitamin K deficiency
which vitamins are fat soluble
causes of K deficiency
* 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
27
symptoms of vitamin K deficiency
treatment
* haemorrhage- epistaxis, sound, GI malaena
* easily bruises
* small clotes under the nails
phytonadione
28
Von Willebrand disease
what does vWf do?
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
29
vWillebrand disease
symptoms
diagnosis
which antibiotic can cause it
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
30
Form a differential diagnosis for someone presenting with tiredness
\<1 month
chronic
***_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
31
diabetes
which population is type 1 more frequent in?
complications of both types of diabetes?
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
32
diagnosis of DM
**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
33
alternative causes for hyperglycaemia
**_Pancreatic diseas_**e: 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
34
T1DM
## Footnote
AKA?
what % of DM cases?
patho?
epidemiolgy?
associated with what?
* 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
35
symptoms of T1DM?
* **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
36
treatment of T1DM
* 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
37
***_T2DM_***
what % of DM cases?
patho?
linked to what?
acquired or inherited?
causes (2)
* 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
38
symptoms of T2DM
***_Symptoms_***
* Polydipsia
* Polyuria
* Blurred vision
* Unexplained weight loss
* Recurrent infections
* Tiredness
s***_igns_***
*_Acanthosis nigricans_*: dark pigmentation of skin folds insulin resistance
Presence of risk factors
39
risk factors for T2DM
* 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)
40
treatment for T2DM
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
41
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42
how does renal disease present? (2)
1. asymptomatically
2. renal tract symptoms
43
how do you detect renal disease in
1. asymptomatic presentation
2. renal tract symptoms
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
44
***_Acute renal disease (AKI)_***
what is it? how is it measured?
definition by diagnosis?
= 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
45
how do you stage an AKI?
risk factors for an AKI
serum creatinine vs urine output
* Pre-existing CKD
* Age
* Male
* Comorbidity (DM, cardiovascular disease, malignancy, chronic liver disease, complex surgery)
46
symptoms of an AKI
Most asymptomatic
* Confusion
* Oliguria – little urination
* Listlessness
* Fatigue
* Anorexia
* Nausea
* Vomiting
* Weight gain
* Oedema
***_Signs of an AKI_***
* R**aised 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
47
causes of an AKI
1. Sepsis
2. Major surgery
3. Cardiogenic shock
4. Other hypovolaemia
5. Drugs
6. Hepatorenal syndrome
7. Obstruction
48
aetiology of an AKI can be split into 3:
***_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
49
Is someone with diabetes more likely to have nephritic or nephrotic syndrome?
Nephritic
50
***_Differential diagnoses_*** of an AKI
* Chronic kidney disease
* Hypoglycaemia DM
* Renal calculi
* Sickle cell anaemia
* Dehydration
* GI bleed
* Heart failure
* UTI
* Protein overload
* DKA
* Urinary obstruction
51
***_Investigations of AKI_***
* **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
52
***_U&Es for kidney injuries/ dysfunction_***
High potassium, high creatinine and high urea
53
what are 2 examples of acute renal diseases?
Nephrotic syndrome
Diabetic Nephropathy
54
***_nephrotic syndrome_***
triad of:
commonest cause in young people?
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
55
***_Aetiology of nephrotic syndrome_***
***_primary renal and secodnary to systemic_***
* ***_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
56
presentation of nephrotic syndrome
***_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
57
investigations for nephrotic syndrome
* **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
58
management of nephrotic syndrome
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???
59
complications of nephrotic syndrome
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
60
***_diabetic nephropathy_***
commonest cause of end stage renal failure
***_diagnosis:_***
***_treatment:_***
***_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
61
***_CKD_***
## Footnote
causes:
Rfx:
presentation:
***_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
62
investigations for CKD
complications
* 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
63
ddx CKD
what investigation must be done before a renal biopsy
***_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
64
***_Glomerulonephritis_***
Includes nephritic and nephrotic syndrome. What is the difference?
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
65
haematuria ddx:
*_Renal causes_*
* Glomerulonephritis
* IgA nephropathy
* Polycystic kidney disease
* Sickle cell disease
* Haemophilia
* Malignancy--\> kidney,
*_Urinary tract_*
* Malignancy--\>ureter, bladder
* Calculi (stone)
* UTI
66
***_Hypothalamic-pituitary-adrenal axis_***
Out of T3 and T4, which in converted into which?
![]()
## Footnote
t4 --\> T3
67
What is thyroxicosis
who is it much more common in
causes
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
68
hyperthyroidism effect on TSH FT4 and FT3
causes
**(↓****TSH /↑********FT4 /** **↑****FT3)**
**causes**
* Grave’s disease
* Toxic adenoma, Toxic MNG
* Thyroiditis
* Amioderone
69
pituitary stimulation effect on TSH FT4 and FT3
causes
↑TSH / ↑FT4 / ↑FT3)
* TSHoma
70
Excessive Exogneous Thyroid hormones (¯TSH / ¯ FT4 / FT3)
Amiodarone excess
71
Symptoms of hyperthryoidism
* **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
signs of hyperthyroidism
* 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
tests for hyperthyroidism
* ↓TSH and TRH (supressed) due to negative feedback effect of T3 and T4)
* Thyroid autoantibodies
* Isotope scan
* Test visual fields in ophthalmopathy
74
treatments for hyperthyroidism
1) ***_Drugs_***: B-blockers e.g., propranolol for rapid control of symptoms
***_Antithyroid medicatio_***n
a) **titration method**- c**_arbimazole_**/ (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
complications of anti thyroid drugs
* 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
Hypothyroidism (myxoedema)
causes
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
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Symptoms of hypothyroidism
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
signs of hypothyroidism
***_Signs_*** BRADYCARDIC
* Bradycardic
* Slow reflexes
* Ataxia
* Dry thin skin
* Yawning/ drowsy
* Cold hands
* Round puffy face
* Defeated demeanour
* Immobile ileus
* CCf
79
treatment of hypothyroidism
Levothyroxine (T4)
Amiodarone (iodine rich drug)
80
what is adrenal insufficiency
what are the effects of cortisol
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
causes of secondary adrenal insufficiency
- 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
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***_Addison’s disease_***
what is it and who does it affect
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
risk factors for addisons
***_Risk factors_***
* Have cancer
* Anticoagulants
* Chronic infections like TB
* Adrenalectomy
* Comorbid autoimmune disease t1dm or Graves’
84
causes of primary hypoaddrenalism
• 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
***_Clinical features of primary hypoadrenalism/ Addison’s disease_***
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
lab tests for addisons
- ↓Na+ / ↑K+ (as a result of ↓in mineralocorticoids)
- ↑Urea
- Mild ↑Ca2+
- Anaemia (normocytic, normochromic unless B12 deficiency)
87
adrenal insufficiency diagnosis
ACTH levels
synacthen test long or short
88
treatment for adrenal insufficiency
* 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
90
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***_Addisonian crisis / acute adrenal crisis_***
***_clinical features_***
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
***_Management_*** of an addisonian crisis
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
Cushing's--\> adrenal excess
the adrenal gland produces 3 kinds of hormone:
what is cushings syndrome and what is the chief cause
*_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
2 classifications of Cushing's cause
**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
symptoms of adrenal excess// cushings
* Fatigue
* **Lethargy**
* **Proximal muscle weakness**
* **Peripheral oedema**
* **Weight gain**
* Depression, mood swings, insomnia
* Irregular periods
* Reduced libido
* F**acial plethora** (redness)
* Buccal hyperpigmentation (black)
* Headaches and visual field defects if pituitary adenoma
96
Clinical signs of Cushing's
differential diagnosis
* 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
how to confirm cushings syndrome
* **Overnight dexamethasone suppression tes**t- 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
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***_How to identify cause of cushings syndrome_***
***_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
management of cushings
definitive treatment is surgical (trans-sphenoidal surgery, bilateral adrenalectomy)
medical (metyrapanone)
radiotherapy
101
psuedocushings
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
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what is anaemia
diagnostic amount
why may Hb be low?
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
symptoms of anaemia
* Fatigue
* Dyspnoea
* Faintness
* Palpitations
* Headache
* Tinnitus
* Anorexia
Angina If pre-existing coronary artery disease
104
anaemias can be grouped into 3 by their relative size MCV
what are the causes of each
***_Microcytic anaemia- LOW MCV- TAILS_***
1. **T**halassaemia- really low MCV despite raised RBC
2. **A**naemia fo chronic disease
3. **L**ead poisoning
4. **I**ron deficiency anaemia- most common cause
5. **S**ideroblastic 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
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iron deficiency anaemia
causes
signs tests
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
treatment for iron deficiency anaemia
ferrous sulfate
107
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what is the difference between acute and chronic leukaemia
**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
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Acute lymphoblastic leukaemia
which mature cells are affected
more common in kids or adults?
* 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
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***_Signs and symptoms of ALL_***
***_tests for ALL_***
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
treatment for ALL
_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
***_Acute myeloid leukaemia_***
how fast is progression?
kids or adults?
Rapid progression
Neoplastic proliferation of myeloid blast cells
Most common acute leukaemia in adults
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***_Signs and symptoms of CML_***
***_diagnosis of CML_***
***_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)
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CML
* occurs most frequenlty in which groups
* presence of which chromosome in \>80%
* symptoms
* tests
***_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
CLL
## Footnote
***_what is the hallmark of this cancer?_***
***_symptoms_***
***_signs_***
***_tests_***
***_complications?_***
***_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
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how does carcinoma of the oesophagus cause weight loss?
* **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
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Why does cancer lead to weight loss
* 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
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causes of malabsoprtion (context: understand how malabsoprtion can lead to weight loss)
***_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
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symptoms of malabsorption disorders
***_Symptoms:_***
* Diarrhoea
* ¯Weight
* Lethargy
* Steatorrhea
* Bloating
***_Resultant deficiency signs_***
* Anaemia Fe, B12, folate
* Bleeding disorders K+
* Metabolic bone disease vit D
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when should you suspect coeliacs?
coeliacs is associated with?
coeliac disease has a 6x higher chance in?
***_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
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presentation of coeliacs
***_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
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how is coeliacs diagnosed?
* Hb (\<130 in men, \<120 in women)
* ¯ B12, Ferritin
* Antibodies--\> anti-transglutaminase
* Duodenal biopsy (villous atrophy, inter-villous WBCs, crypt hyperplasia)
124
125
ulcerative colitis and crohn's disease comparison
* location of inflammation
* pattern of inflammation
* appearance of inflammation
* location of pain
* bleeding
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Crohn's disease
* how many layers does granulation affect?
* how far up the gI tract does crohns affect?
* is this inflammation continuous?
epidemiology
* Chronic inflammatory disease characterised by **transmural granulomatous** affecting **any part of the GI trac**t 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
symptoms and signs of crohn's disease
***_Symptoms:_***
* Diarrhoea
* Abdominal pain
* Weight loss
* Fatigue
* Fever
* Malaise
***_Signs_***
* Bowel ulceration
* Abdominal tenderness
* Perianal fistula/ skin tags/ anal strictures
128
Complications and tests for Crohns
***_Complications_***
* Small bowel obstruction
* Abscess formation
* Fistulae (e.g., colo-vaginal)
* Malnutrition --\> makes your bowel leaky --\> lack enough protein to make albumin
* Perforation
129
tests and treatment for Crohn's
***_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 **glucocorticoid**s (**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
what are the 6 F's of abdominal swelling?
* Fat
* Fluid
* Foetus
* Flipping big mass
* Flatulence
* Faeces
131
What blood product is used to correct clotting disorder?
which group is the universal:
blood donor?
blood recipient?
plasma donor?
plasma recipient?
fresh frozen plasma
## Footnote
blood donor- O-
blood recipient AB+
plasma donor AB
plasma recipient O
132
who requires irradiated blood?
* Hodkins disease
* Recipients of autologous stem cell transplants
* Allogenic stem cell transplant
* Congenital immunodeficiencies: SCID
133
symptoms of transfusion reaction
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
symptoms of acute haemolytic reaction
* Agitation
* Fever rapid onset
* Hypotension
* Flushing
* Chest pain
* ***_TRALI_*** (transfusion related acute lung injury)
* Dyspnoea
* Cough
* White out
135
nephrotic syndrome effect on electrolyte and water balance
effects of acute malnutrition
hypoalbuminaemia--\> oedema
***_acute malnutrition_***
* Kwashiorkor- protein deficiency
* Bilateral pitting oedema
* Distended abdomen
* Hair thinning
* Skin/ hair depigmentation
* Dermatitis
136
***_what is conn's syndrome_***
## Footnote
*_What kind of hormone is Aldosterone?_*
*_Action of aldosterone?_*
*_What is the name for primary hyperaldosteronism?_*
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
*_Causes for primary hyperaldosteronism/ Conn's_*
*_what is Secondary hyperaldosteronism_*
*_Causes of secondary hyperaldosteronism_*
*_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
Signs and symptoms
* **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
investigations for hyperaldosteronism
* 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
DDx of hyperaldosteronism
management of primary and secondary
* 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
what is considered to be hypertensive
what are secondary causes of hypertension
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
* what is malnutrition
* what is the difference between kwashiorkor and marasmus
* what is the link between malnutrition and immune function
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
acromegaly
* cause
* patholhysiology
* symptoms
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
signs of acromegaly
***_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
complications of acromegaly
tests for
diagnosis
***_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
treatment for acromegaly
name 2 conditions that can cause abdominal pain
name 2 diseases that can cause loose stools
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
DDX causes of vomiting
* GI
* CNS
* Metabolic
* Alcohol and drugs
***_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
***_Acute pancreatitis_***
characterised by what
what percentage is mild vs severe
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
causes of acute pancreatitis
get smashed
1. all stones (~35%)
2. thanol (~35%)
3. rauma
1. teroids
2. umps
3. utoimmune
4. corpion venom
5. yperlipidaemia, hypothermia, hypercalcaemia
6. RCP and emboli
7. rugs
150
symptoms of acute pancreatitis
## Footnote
***_Signs_*** of acute pancreatitis
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
tests for acute pancreatitis
management
* **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
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what is a Ba meal used for?
Barium meal is a diagnostic test used to detect abnormalities pf the oesophagus, stomach and small bowel using x ray images
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DDx causes of weight loss
**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
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differential diagnoses for cause of weight gain
**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
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a lump in the neck makes you think of:
tiredness makes you think of:
* Goitre- hyper/ hypothyroidism
* Lymphadenopathy- infective (TB, EBV, HIV), sarcoidosis, amyloidosis, Rheumatoid, **Chronic Lymphyocyte Leukaemia**
***_Tiredness makes you think of:_***
Cushing’s Syndrome
Anaemia
Hypothyroidism
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what are the health risks associated with weight gain?
* T2DM
* Coronary heart disease
* some types of cancer
* stroke
* heartburn
* sleep apnoea
* osteoarthritis
* COVID-19 symptoms
* hypertension
* dyslipidaemia
* gallbladder disease
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gravitational petechial rash makes you think of
thrombocytopaenia
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definition of shock
signs of shock
***_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
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***_Management of shock from Addisonian crisis_***
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
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fluid assessment
* 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
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***_Metabolic acidosis causes:_*** ↓pH ↓HCO3
* lactic shock (shock, infection, tissue ischaemia)
* urate (renal failure)
* ketones (diabetes mellitus, alcohol)
* drugs/ toxins (salicytes, methanol)
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causes for metabolic alkalosis ↑pH ↑HCO3-
Vomiting
K+ depletion
Burns
Ingestion of base
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resp acidosis
resp alkalosis
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
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hypernatraemia presentation and causes
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)
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hyponatraemia
presentation
* anorexia
* nausea
* headache
* irritability
* confusion
* weakness
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hyperkalaemia presentation and causes
***_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
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hypokalaemia
signs and symptoms
causes
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
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what is the first line initial bets test for diagnosing Cushing's
overnight dexamethosone suppression test.
dexamethosone is a steroid like cortisol. by increasing serum steroid, you see if the pituitary gland stops secreting acth.
