miscellaneous Flashcards
How do you treat Status Epliptious?
1) ABCDE
2) Lorazepan 4mg IV or 10mg Diazepam PR
3) identify and reverse any underlying cause
4) if contine longer than >30min = phenytoin infusion (15mg/kg @ 50mg/min) and an anaethetist for GA and ITU admission
How do you treat Anaphylaxis?
ABCDE Adrenaline IM Adults 500 micrograms of 1:1000 Children >12 500 micrograms Children 6-12 300 micrograms Children < 6 150 micrograms
What is the definition of AKI?
A rapid decrease in renal function
leads to a fluid/electrolyte imbalance and acid/base disturbance.
RF= age, co-morbidities and medication
Causes of AKI?
PRE-RENAL: Sepsis Hypotension Hypovalemia Renal artery stenosis cardiac liver ACEi
INTRINSIC:
Vasculitis
Glomerulonephritis
Tubular Necrosis
POST-RENAL:
renal tract obstruction (has to be bilateral damage or chronic kidney damage)
What is nephrotic syndrome?
Oedema, Protein Urea, hypoalbuminaemia and hyperlipidemia
Over 3.5g of protein
Causes of nephrotic syndrome?
Deposition Disease Minimal Change Disease Focal and Segmental Glomerulosclerois Membranous Nephropathy Membranoproliferative GN Myeloma ( screen in CKD if >50yrs)
What is type 1 rapidly progressing glomerulonephritis?
Anti-GMB glomerulonephritis
What causes type 1 RPGN?
Good Pasteure’s Disease
Anti-GBM disease (same as good pasteures but involves only kidney)
What is good pasteure’s?
Anti-glomerular basement membrane disease + pulmonary haemorrhage.
Caused by an anti-body to the alpha-3 chain of type IV collagen
15% of goodpasture’s syndrome is AGBM disease and the rest is ANCA vasculitis
What is type 2 glomerulonephritis?
Deposition of immune complexes
Causes of type 2 glomerulonephritis?
SLE, acute proliferative glomerulonephritis and IgA nephropathy, Henoch-Schonlein pupura.
What is type 3 glomerulonephritis and the causes?
Vasculitis.
Glomeruli are damaged in an undefined manner perhaps through the activation of neutrophils in response to ANCA.
Isolated to glomerulus= primary
Systemic= secondary = ANCA associated vasculitis, granulomatosis with polyangitis, microscopic polyangitis.
What is IgA nephropathy?
Non-aggressive IgA= traditionally slow progression to CKD
Often get episodic haematuria following a sore throat (strep A)
can develop into RPGN
Aggresive IgA= nephritic syndrome 1-4 days post strep A infection
What is post infectious GN?
Get nephritic syndrome several weeks post Strep A infection.
Causes of Jaundice
PRE-HEPATIC
Haemolysis (unconjugated)
INTRINSIC: Gilberts (unconjugated) Viral Hepatitis Drugs Alcoholic Hepatitis Cirrhosis Pregnancy Recurrent Idiopathic Cholestasis Infiltrations Congenital
POST HEPATIC: Common duct stones Carcinoma (bile duct, pancrease,ampulla) Biliary stricture sclerosing cholangitis Pancreatitis Pseudocyst
Long term consequences of CKD?
Reduced GFR= Raised K+ and Creat
Acidosis (reduced acid removal)
reduced EPO secretion= anaemia
renal bone disease- reduced Ca, Increased Phosphate, increased parathyroid (2ndary hyperparathyroidism)
impaired BP regulation- HTN
reduced fluid removal- oedema
impaired iron absorption- iron deficiency
reduced clearance of gastrin- peptic ulceration
Causes of CKD?
PRE-RENAL:
RAS (discrepency of >1cm in kidney size think) , nephrosclerosis + ACEi
RENAL:
GN, TIN (tubulointerstital Nephritis), ADPKD
POST- RENAL
BPH, RPF (renal blood flow)
What is Addison’s disease and how would you diagnose?
hypocortisol and adrenal insufficiency
Measure 8am cortisol- Low = adrenal insufficiency
Cosyntropin stimulation test: measure base ACHT test.
administer synacthen (synthetic ACHT)
low cortisol+ high ACTH= primary (adrenals)
low cortisol + low ACTH= secondary (pituitary)
Causes of lymphadeonopathy?
REACTIVE:
Infective: Bacterial (tonsillitis, cellulitis, TB, primary syphillis), Viral (EBV, CMV, HIV, hepatitis), Other (toxoplasmosis)
Non-infective: Sarcoidosis, amyloidosis, connective tissue disease (RA, SLE), dermatological (eczema, psorasis), drugs (phenytoin, retroviral drugs)
INFILTRATIVE:
Benign Histiocytosis
Neoplastic: Haemotological ( Hodgekins, Non-hodgekins lymphoma, CML,CLL, ALL,AML)
Causes of hepatomegaly?
SMOOTH AND TENDER: alcoholic hepatitis, Tricuspid regurgitaion w/RHF. Infectious Hepatitis ( acute infection) , RHF/PE, Glandular Fever, Budd-Chiari Syndrome, Abcess.
SMOOTH BUT NOT TENDER: Amyloidosis, leukaemia, early cirrhosis, lymphome, haemochromatosis, Primary Biliary Cholangitis, Fatty Liver, HIV, Sarcoidosis
IRREGULAR AND NON-TENDER: Neoplastic ( Hepatoma, metastatic carcinoma), hyatid cyst, polycystic liver
Causes of splenomegaly?
FEVERS: Infection (malarie, IE, hepatitis, EBV,TB, CMV, HIV), sarcoid, malignancy (lymphoma, chronic leukaemia)
LYMPHADENOPATHY: Glandular Fever, leukaemias, lymphomas, Sjogren’s Syndrome
PURPURA: Amyloid, Septicaemia, Typus, DIC, Meningiococcaemia
ARTHRITIS: Sjogren’s, RA, SLE, Lyme’s Disease, Vasculitis
ASCITES: Carcinoma, Portal Hypertension
MURMUR: IE, Rhuematic Fever, Hypereosinophillic syndrome, amyloid
MASSIVE SPLENOMEGALY: Malaria, CML, myelofibrosis, leishmaniasis, Gaucher’s
WEIGHT LOSS AND CNS PATHOLOGY:
Cancer, lymphoma, TB, myeloma, arsnic poisoning
ANAEMIA: Haemolytic Anaemia, leishmaniasis, leukaemia, pernicious anaemia.
Causes of hypercalcaemia?
ENDOCRINE:
Excess PTH: Primary and Tertiary Hyperparathyroidism, Ectopic Parathyroid Hormone
Other: Thyrotoxicosis and Addison’s Disease
MALIGNANT: Myeloma, Bone Mets
EXCESS ACTION OF VIT D: lymphoma, granulomatous disease (sarcoid/TB), self administered Vit D
DRUGS: Thiazides, Vut D analogues, Lithium and Vit A
OTHER: long term immobility, familial hypocalciuric hypercalcaemia.
What is IgA vasculitis?
Systemic Also known as HSP Triad of abdo pain, Purpura and arthritis most common vasculitis of childhood get purpuric rash on legs and buttocks can cause intersusseption can cause nephritic syndrome can get IgA nephropathy
