All notes Flashcards
Do type 1 diabetes present acutely with ketosis?
Yes
Symptoms of Diabetes
Tiredness, lethargy
Polyuria and polydipsia–
Glucose SLOWLY rises further
With other co-morbidities it become difficult to drink enough–Osmotic diuresis causes loss of water and a rise in sodium–EVENTUALLY the glucose is VERY high, as is the sodium
How do you calculate Ion gap?
+ve + -ve = osmolality
What are the microvascular complications of diabetes? How?
Retinopathy
Nephropathy
Neuropathy
Glycosylation of basement membrane proteins - leaky capillaries
What are the microvascular complications of diabetes?
Dyslipidaemia, hypertension, hypercholesterolaemia
Leads to:
–IHD–CVA–Peripheral gangrene
What do features are there on diabetic retinopathy
Hard exudates (cholesterol) •Microaneurysms (“dots”) •Blot haemorrhages
Treatment for background diabetic retinopathy?
Improve blood glucose control
What does ischaemia of the eye cause? Why is that bad?
New vessels to grow
Blindness
Management of diabetic retinopathy (proliferative and pre proliferative)
Cotton wool spot - suggests ischaemia
Pan retinal photocoagulation
Management of hyperglycaemia (in order)
Diet and exercise
•Biguanide (Metformin)
•Sulphonylureas (eg gliclazide)
•Insulin sensitisers : thiozolidinediones such as rosiglitazone or pioglitazone
•Insulin itself (there are several new insulin analogues now available)
•Incretins (GLP-1 analogues)
•Gliptins (Dipeptidyl peptidase 4 inhibitors)
Examples of insulin analogues
Long acting - zinc suspension
Short acting - insulatard and actrapid
Advantages of using insulin
Can give best control of HbA1c when combined with diet and exercise.
•No side effects (compared to : )
•metformin (diarrhoea)
•SU (occasional reactions) •thiazolidinediones (rare hepatic, ?osteoporosis
Disadvantages of using insulin
If you drive HGV, cannot work •(exenatide exempt) •Hypoglycaemia common with good control •Weight gain •Increased insulin as a consequence •Huge doses required in patients with type 2 diabetes
Affects of GLP1
Increased insulin
Reduce gastric emptying
increased hypothalamic satiety
Examples of GLP1 analogues
exanatide
liraglutide
semaglutide
Do SGLT2 inhibitors have a cardiovascular benefit
Yes
On kidney
Signs of diabetic nephropathy
Hypertension
Increased proteinuria >3000g
Renal failure
Histological signs
Histological features of diabetic nephropathy
Glomerular - mesangial expansion, basement membrane thickening, glomerulosclerosis
Epidemiology of diabetic nephrology
Age
racial factors
loss of cv morbidity
Stages for treatment of D. Nephro
Diabetic control
•Blood pressure control
•Inhibition of the activity of RAS system
•Stopping Smoking
When and when not should you use a ACE inhibitor for diabetic nephropathy
decrease microalbinuria
prevent end stage renal failure
causes hyperkalaemia
do not give for renal artery stenosis
Signs of renal failure
Electrolyte misbalance–Hyperkalaemia, hyponatraemia
- Acidosis
- Fluid retention
- Retention of waste products–Small molecules, e.g., urea, creatinine, urate–Phosphate–Middle molecules, e.g., peptides, ß2‐microglobulin
- Secretory failure–Erythropoietin –1.25 vitamin D
Symptoms of renal failure
Symptoms–Tiredness, lethargy–Shortness of breath, oedema–Pruritis, nocturia, feeling cold, twitching–Poor appetite, nausea, loss of/nasty taste, weight loss
- Anaemia –exacerbates tiredness
- Renal bone disease –aches & pains, pruritis
What happens if no renal replacement treatment is given for renal failure?
Hyperkalaemia –arrythmias, cardiac arrest–Pulmonary oedema–Nausea, vomiting–Malnutrition / cachexia–Fits–Increasing coma–DEATH
Types of renal replacement therapy
Peritoneal dialysis
Haemodialysis
Transplant
When do you give Renal replacement therapy?
When gfr goes below 10
Benefits of dialysis
Improve symptoms
correct fluid balance
no acidosis, hyperkalaemia, pulmonary oedema caused by resistance to diuretics
Risks of dialysis
Infection, hypotension/ arythmias (h), access
work, family, travel
What does dialysis not treat
Getting old
•Lack of erythropoietin–Anaemia
•Lack of 1.25 vitamin D–Hyperparathyroidism–Renal bone disease
•Other diseases –comorbidities–SLE–Diabetes–Vascular disease
Pros and cons of transplants
Transplantation
BENEFITS
•Better renal replacement
•Improvement in metabolic disorders–Anaemia–Renal bone disease
•Costs less in long‐term
•Prolonged survival
•Quality of life–Avoids disadvantages of HD/PD–Much easier to travel, work, maintain independence
RISKS
•Older and sicker patients not eligible
•Immunosuppression–Increased infection–Increased malignancy
•Not a cure–Surgical complications–Hospital visits –particularly frequent at start
•Often worse off if/when transplant fails
Resp failure
Low O2
1 - normal/low co2 - V/Q mismatch
2- high co2 - hypoventilation
How do you assess a acutely unwell patient?
Callforhelp!!
Airway–Patent?,Stridor?Obstructed?–IFyes2222
Breathing - Speech(fullsentences?),RR,Sats,ABG,auscultation,CXR
Circulation–HR,BP,CRT,ECG
Disability–GCS,Glucose,Pupils,Neuro-exam
Exposure/Everythingelse–Abdomen,Signsofoverload
Re-assess!!!!
Define asthma
Chronic inflammatory airway disease characterised by reversible airways obstruction
What do you give for low sats and high resp rate in an acute situation?
oxygen,salbutamolnebulisers,steroids,magnesiumandreassess
What is a moderate asthma attack?
PEF at 50-75% of best or predicted•No signs of severe asthma
Severe asthma attack
PEF at 33-50% of best or predicted
•respiratory rate ≥25/min
•heart rate ≥110/min
•Inability to complete sentences in one breath
Signs of life threatening asthma
CHEST
Cyanosis -SpO2 <92%, PaO2 <8 kPa •Hypotension •Exhaustion –Poor inspiratory effort, Confusion, Normal PCO2 •Silent chest •Tachy-/Brady-Arrhythmias
How do you manage life threatening asthma
ABCDE
severe - 98% sats, bronchodilators (SABA +/- ipratropium, IV magnesium
Steroids: PO prednisolone/IV Hydrocortisone
-> if improved - TAME (technique, avoid triggers, monitor PEF and educate - discharge if > 75%)
If severe/ not get better
- help
- same treatment
Levels of COPD
Mild FEV1 >80% predicted
•Moderate FEV1 50-80% Predicted
•Severe –FEV1 30-50% Predicted
•Very severe –FEV1 <30% Predicted
What is COPD
Minimally reversible airflow obstruction characterised by an FEV1/FVC ratio of <0.7
How do you manage acute COPD
ABCDE
T2RF - sats 98%, salbutamol,ipratropium,
steroids: OD prednisolone, hydrocortisone IV
No for T2RF - lower sats (94-98 or 88-92 with Venturi) same med. - may need ABs
Improved - check sputum, wean off, smoking cessation, inhaler technique
What is BIpAp
Bi level CPAP
Helps with breathing in and out
Risk factors for DVT/PE
Risk factors •Immobilisation •Malignancy •Recent Surgery •HRT/COCP •Thrombophilias
Gold standard for PE
CT pulmonary angiogram
Scoring systems for PE
Wells and geneva
Signs of right heart strain on a ECG
Deep S wave - lead 1
Deep q waves - lead 2
T wave inversion - lead 3
Occuled pulmonary circulation
How do you manage acute PE?
HS - yes - help, oxygen, fluids, assess for thrombolkysis or percutaneous embolectomy
HS - no - Hestia, PESeverity index, sPESI - high risk - LMWH, oxygen
- low risk - discharge high does LMWH, DOAC and warfarin for three months
What is acute pulmonary oedema?
Accumulation of fluid in lung parenchyma - impaired gas exchange
Causes of pulmonary oedema
Cardiogenic –Heart Failure, Arrhythmia, Myocardial Infarction
•Renal –Acute, severe Kidney failure
•Acute respiratory distress syndrome (ARDS) –Caused by lung injury, i.e. infection (Cov-Sars-2
Management of Acute cariogenic po
ABCDE - sit up
- oxygen, IV diuretics - furosemide, beta blockers if arrhythmia
- consider nitrate infusion if systolic above 100 + CPAP - drives out fluid
Record weight every day
X ray changes for a tension pneumothorax
tracheal deviation away from affected side
mediastinal shift away
loss of lung markings on affected side (air)
Treatment of PT
Emergency needle decompression
high flow oxygen
chest drain
1 - >2cm - aspirate, less = discharge
2- >2cm - chest drain, less aspirate and admit
Issues with obstructive sleep apnoea
Intermittent hypoxia and sleep disruption
How do you measure sleep?
ear sleep monitor
How do you treat OSA
CPAP - moderate to severe with symptoms of sleepiness
Main risk factor for OSA
Obesity and narrowed airway
What is a normal GFR
> 90ml/min
Main symptoms of renal problems
Haematuria •Proteinuria•Nephrotic syndrome•Nephritic syndrome•Hypertension•Acute kidney injury•Chronic kidney disease•Urinary tract infection•Abdominal pain•Complications of hypertension (esp malignant hypertension)•Oliguria or anuria•Polyuria, nocturia
Functions of the kidney
filtration and excretion electrolyte homeostasis hormone production - epo, vit d blood pressure control acid base homeostasis
How do you treat acidosis?
Bicarbonate
What factors affect GFR
age, sex, body size, muscle mass
reduced = loss of filtering capacity and accumulation of waste products
Test for blood and protein in urine
urine dip
Colour of urine and problem
red/brown - myoglobinuria/haemoglobinuria
- food dyes, rifampicin (TB)
white - pyuria, phosphate crystals, chyluria
black - haemoglobinuria, alkaptonuria
What does AKI mean
rapid decline in renal function over hours/days
accumulation of wast, metabolic consequences, can have reduced output
rise of serum creatinine by 26ml/mol in 48 hrs or 1.5x reference value or urine output less than 0.5ml over 6 hrs
staged based on severity
RF for AKI
risk
ill
surgery
e.g. ensuring adequate hydration is a preventative measure
Recognised risk factors for AKI•Age >75 years•Pre-existing CKD (eGFR <60 mL/kg/1.73 m2)•Previous episode of AKI•Debility and dementia•Heart failure•Liver disease•Diabetes mellitus•Hypotension (Mean arterial pressure <65mmHg, systolic BP <90mmHg)•Sepsis•Hypovolaemia•Nephrotoxins, eg gentamicin, NSAIDs, iodinated contrast•Continued antihypertensives in setting of hypotension, eg ACE inhibitors, loop diuretics
Pre renal causes of AKI
Hypovolaemia
low cardiac output
hypotension
renal artery thrombosis
Renal causes of AKI
Acute tubular necrosis Glomerulonephritis Vasculitis Nephrotoxins, contrast, rhabdomyolysis Interstitial nephritisHUS/TTP Malignant hypertension Myeloma
Post renal causes of AKI
Ureteric obstruction
Urethral obstruction
Blocked urinary catheter
Bladder tumour
Difference between AKI and CKD
AKI is reversible
CKD - impaired, progressive, eskd, not reversible
How do AKI present
non specific symptoms
uraemia (nausea, vomiting and anorexia)
decreased urine output
systemic features (rash, myalgia, arthralgia, headaches)
urea and cr up
acidosis, hyperkalaemia, salt and water retention
For UTI history what should you check
duration systemic features PMx - vascular, childhood renal, UTI, diabetes, hypertension stroke early death herbal, recreational drugs
How to distinguish between a pre renal, glomerular and tubular AKI in urine?
G: red cells, proteinuria
T: minimal blood, less protein, white cell case
Pre-renal - no blood nor protein
Things you always want to know with renal patients
baseline creat take an ABG for hypoxia and acidosis electrolyte US - kidney size CXR - for fluid overload, chest infection urinalysis
Common causes of AKI
Acute tubular necrosis functional myeloma Acute tubular interstitial nephritis athero embolic rhabdomyolysis
Need to find a treatable cause for AKI - so what investigations should you do?
volume status (for ATN) •Urine microscopy and dipstick •Imaging (U/S) *** Obstruction *** •ANCA, Anti-GBM, SLE immunology (ANA, dsDNA, complements) •Creatinine kinase•FBC, clotting •Inflammatory markers •Myeloma screen (protein electrophoresis, urine BJP) •May need biopsy
How do you treat:
- hyperkalaemia
- PO
- acidosis
- hypertension
- uraemia (damages brain, nerves and heart)
IV calcium
insulin and dextrose
nebulised salbutamol
dialysis
What is CKD
syndrome with a cause for renal
kidneys usually smaller
slow progression for eskd
5 stages of CKD and action
1 normal >90 2 60-89 kidney damage 3 30 - 59 moderate decreasing gfr 4 15-29 - severe - prepare transplant 5 less than 15 = kidney failure - dialysis
if macroalubinuria is present - worsening kidney function
RF for CKD
ElderlyHypertensionDiabetesIHDFamily History CKDAfrican AmericanObesity
Main causes of CKD
Diabetes Chronic glomerulonephritis vascular diseases IHD, HTN Autosomal dominant PKD childhood infections
How to prevent progression of CVD in CKD patients
BP control - ACEi ARB max doses - need a low blood pressure, reduce proteinuria (SGLT) - glifozins
no smoking
exercise, low salt and protein diets
avoid nephrotoxins like NSAIDS
What drug slows the progression of kidney disease
Glifozins - SGLT2 inhibitors
Triad for nephrotic syndrome
proteinuria, oedema, hypoalbuinaemia
Gold standard for finding out proteinuria problem
Renal biopsy
Do US first
Main causes of proteinuria and nephrotic syndrome
Diabetes Minimal change disease membranous nephropathy amyloid SLE
Tests for proteinuria
protein:creatinine ratio
serum albumin and cholesterol
serum creatinine
glucose, SLE tests, virology (Hep B, C and HIV), myeloma screen
Protein uria management
Control oedema - low salt diet, diuretics
ACEI and ARB
Steroids
How does Haematuria present
Pain (stones/cancer)
Age > 40 - cancer - cystoscopy
below 40 glomerular cause
Most common haematuria glomerular causes
Alports - basement membrane disease
IgA nephropathy
When are neutrophils raised
acute inflammation
When are lymphocytes and plasma cells raised
chronic inflammation
lymphomas