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Metabolic

1
Q

Cancers curable with chemotherapy

A 
Teratoma
Seminoma
High grade Hodgkin's lymphoma
Wilm's
Myeloma
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2
Q

Cancers with no gain for chemotherapy

A

Melanoma
Renal
Cholangiocarcinoma

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3
Q

MOA of cytotoxics

A

Antimetabolites: 5FU, gemcitabine, capectiabine

Alkylating agents: cyclophosphamide, cisplatin, carboplastin

Mitotic spindle poison: vincristine

Taxanes: paclitaxel, docetaxel

Modify tertiary structure of DNS: etoposide

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4
Q

Short term side effects of chemotherapy

A

Nausea and vomiting

Anorexia

Weight loss

Alopecia

Bone marrow suppression - neutropaenia, anaemia, thrombocytopaenia

Infective symptoms

Fatigue

Liver and renal toxicity

Mucositis

Peripheral sensory neuropathy

Ototoxcity

Acute cardiomyopathy

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5
Q

Long term side effects of chemotherapy

A

Cardiomyopathy

Pulmonary fibrosis

Increased risk of secondary cancers, particularly Hodgkin’s, acute leukaemia, testicular cancer

Subfertility/infertility

Renal insufficiency

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6
Q

Why are brain tumours hard to treat with chemotherapy

A

Chemotherapy is a large molecular with low solubility.

BBB is lipid soluble and small molecules.

Can’t cross the BBB to treat
Brain tumours also poorly irrigated.

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7
Q

When chemotherapy can be given?

A

Primary chemotherapy - sole anti cancer treatment if highly sensitive tumour types

Adjuvant - given after surgery to mop up microscopic disease

Neo-adjuvant - given pre-surgery to shrink the tumour

Concurrent - given with radiation

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8
Q

Hormonal chemotherapy therapies

A

Usually reserved for breast and prostate cancer.

Highly effective and relatively non-toxic.

Breast cancer:

  • If oestrogen receptor positive, oestrogen binds to cells to increase growth
  • Tamoxifen (SERM) competes for this binding to stop growth
  • Aromatase inhibitors prevent precursors being converted into oestrogen

Prostate cancer:

  • Androgens are a critical growth factor for prostate cancer
  • Goserelin - LHRH agonist - reduces pituitary production of LH and FSH
  • Flutamide anti-androgen, competitive androgen receptor inhibitor

Resistance will eventually develop

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9
Q

Biological chemotherapy agents

A

Work differently depending on the target cell.

Recognise and attach to specific proteins produced by cells.

  • Breast cancer: Trastuzumab (Herceptin) if HER2 +
  • Lymphoma: Rituximab (anti CD20)
  • Colorectal cancer: Cetuximab (EGF receptor)
  • Colorectal, lung and breast: bevactzumab (VEGF)
  • CLL: Alemtuzumab (CD52)
  • Lung cancer: Erlotinib (EGFR-TK mutation)
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10
Q

Insulin

A

Direct replacement for endogenous insulin

Subcutaneous

SE:

  • Hypoglycaemia
  • 
Weight gain
  • 
Lipodystrophy

Used in all patients with T1DM and some patients with poorly controlled T2DM

.

Can be classified according to source (analogue, human sequence and porcine) and duration of action (short, immediate, long-acting).

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11
Q

Metformin

A

Increases insulin sensitivity


Decreases hepatic gluconeogenesis

Oral

SE:

  • Gastrointestinal upset

  • Lactic acidosis*

First-line medication in the management of T2DM.



Cannot be used in patients with an eGFR of < 30 ml/min.

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12
Q

Sulfonylureas

A

Stimulate pancreatic beta cells to secrete insulin

Oral

SE:

  • Hypoglycemia

  • Weight gain
  • 
Hyponatraemia

Examples include gliclazide and glimepiride

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13
Q

Thiazolidinediones

A

Activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake

Oral

SE:

  • Weight gain

  • Fluid retention

Only currently available thiazolidinedione is pioglitazone

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14
Q

DPP-4 inhibitors (-gliptins)

A

Increases incretin levels which inhibit glucagon secretion

Oral

Generally well tolerated but increased risk of pancreatitis

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15
Q

SGLT-2 inhibitors (-gliflozins)

A

Inhibits reabsorption of glucose in the kidney

Oral

SE:
- Urinary tract infection

Typically result in weight loss

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16
Q

GLP-1 agonists(-tides)

A

Incretin mimetic which inhibits glucagon secretion

Subcutaneous

SE:

  • Nausea and vomiting

  • Pancreatitis

Typically result in weight loss

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17
Q

ACTH stimulation test

A

Addison’s disease

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18
Q

Hyperkalaemia

A
  • Acute renal failure
  • Addison’s disease
  • ACE inhibitors
  • Spironolactone
  • Metabolic acidosis
  • Angiotensin 2 receptor blockers
  • Massive blood transfusion
  • Rhabdomyolysis
  • Ciclosporin
  • Renal tubular acidosis (type 4)
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19
Q

Hypernatraemia

A
  • Diabetes insipidus
  • Hyperosmolar non-ketotic diabetic coma
  • Dehydration
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20
Q

Hyponatraemia

A
  • SIADH
  • Addison’s disease
  • Vomiting
  • Thiazides
  • Liver cirrhosis
  • Hypothyroidism
  • Burns
  • Heart failure
  • Diarrhoea
  • Psychogenic
  • Polydipsia
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21
Q

What is paraneoplastic syndrome?

Paraneoplastic syndromes caused by renal cell carcinoma (RCC)?

A

When tumours act as ectopic endocrine organs resulting in over-secretion of hormones.

Paraneoplastic syndromes of RCC:

  • EPO secretion (leads to polycythemia)
  • Renin release (leads to hypertension)
  • PTHrP* (leads to hypercalcaemia)

*Parathyroid hormone-related protein (PTHrP)

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22
Q

Breast cancer tumour marker

A

CA 15-3

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23
Q

Ovarian cancer tumour marker

A

CA 125

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24
Q

Pancreatic cancer tumour parker

A

CA 19-9

25
Q

List all monoclonal antibody tumour markers

A

CA 125 Ovarian cancer

CA 19-9 Pancreatic cancer

CA 15-3 Breast cancer

26
Q

List all tumour antigen tumour markers

A

Prostate specific antigen (PSA) = Prostatic carcinoma

Alpha-feto protein (AFP) = Hepatocellular carcinoma, teratoma

Carcinoembryonic antigen (CEA) = Colorectal cancer

S-100 = Melanoma, schwannomas

Bombesin = Small cell lung carcinoma, gastric cancer, neuroblastoma

27
Q

Alpha-feto protein (AFP) is a tumour marker for what?

A

Hepatocellular carcinoma

Teratoma

28
Q

Carcinoembryonic antigen (CEA) is a tumour marker for which cancer?

A

Colorectal cancer

29
Q

S-100 is a tumour marker for what?

A

Melanoma

Schwannomas

30
Q

What is bombesin a tumour marker for?

A

Small cell lung carcinoma

Gastric cancer

Neuroblastoma

31
Q

Nephrotic syndrome complications?

A

Increased risk of VTE in patients with nephrotic syndrome - prophylactic LMWH required

Increased risk of VTE is a direct complication of nephrotic syndrome.

Other major complications include: increased risk of infections, cardiovascular complications, anaemia, acute renal failure and hypovolaemic crisis.

32
Q

Gardners syndrome

A
  • Autosomal dominant familial colorectal polyposis
  • Multiple colonic polyps
  • Extra colonic diseases include: skull osteoma, thyroid cancer and epidermoid cysts
  • Desmoid tumours are seen in 15%
  • Mutation of APC gene located on chromosome 5
  • Due to colonic polyps most patients will undergo colectomy to reduce risk of colorectal cancer
  • Now considered a variant of familial adenomatous polyposis coli
33
Q

Lynch Syndrome

A
  • Autosomal dominant
  • Develop colonic cancer and endometrial cancer at young age
  • 80% of affected individuals will get colonic and/ or endometrial cancer
  • High risk individuals may be identified using the Amsterdam criteria
34
Q

Amsterdam criteria

A
  • Three or more family members with a confirmed diagnosis of colorectal cancer, one of whom is a first degree (parent, child, sibling) relative of the other two.
  • Two successive affected generations.
  • One or more colon cancers diagnosed under age 50 years.
  • Familial adenomatous polyposis (FAP) has been excluded.
35
Q

BRCA 1 and 2

A
  • Carried on chromosome 17 (BRCA 1) and Chromosome 13 (BRCA 2)
  • Linked to developing breast cancer (60%) risk.
  • Associated risk of developing ovarian cancer (55% with BRCA 1 and 25% with BRCA 2).
  • BRCA2 mutation is associated with prostate cancer in men
36
Q

Li-Fraumeni Syndrome

A
  • Autosomal dominant
  • Consists of germline mutations to p53 tumour suppressor gene
  • High incidence of malignancies particularly sarcomas and leukaemias

Diagnosed when:

  • Individual develops sarcoma under 45 years
  • First degree relative diagnosed with any cancer below age 45 years and another family member develops malignancy under 45 years or sarcoma at any age
37
Q

Prescribing fluids.

Daily potassium requirements?

A

When prescribing fluids, the potassium requirement per day is 1 mmol/kg/day

38
Q

Chemotherapy side effect: nausea and vomiting

A

Risk factors for the development of symptoms include:

  • Anxiety
  • < 50 years old
  • Concurrent use of opioids
  • Type of chemotherapy used

For patients at low-risk of symptoms then drugs such as metoclopramide may be used first-line.

For high-risk patients then 5HT3 receptor antagonists such as ondansetron are often effective, especially if combined with dexamethasone.

Dexamethasone is used to suppress nausea and vomiting with intracranial tumours.

39
Q

Chronic kidney disease: eGFR and classification

A 
Serum creatinine may not provide an accurate estimate of renal function due to differences in muscle. For this reason formulas were develop to help estimate the glomerular filtration rate (estimated GFR or eGFR). The most commonly used formula is the Modification of Diet in Renal Disease (MDRD) equation, which uses the following variables:
serum creatinine
age
gender
ethnicity
40
Q

Factors which may affect the eGFR?

A

Pregnancy

Muscle mass (e.g. amputees, body-builders)

Eating red meat 12 hours prior to the sample being taken

41
Q

RCC late stages complications?

A

The left renal vein can become compressed interrupting the venous drainage of the left testis -left scrotal varicocele.

The tumour can invade the IVC resulting in lower limb oedema.

42
Q

Commonest cancers in men?

A
  1. Prostate
  2. Lung
  3. Bowel
43
Q

Commonest cancers in women?

A
  1. Breast
  2. Lung
  3. Bowel
44
Q

What size stone can pass through ureter and urethra without symptoms?

A

<5mm

45
Q

Symptoms and signs of nephritic syndrome?

A
  • Hematuria
  • Proteinuria < 3.5g/d (protein in the urine)
  • Hypertension
  • Blurred vision
  • Azotemia (increased blood Urea and Creatinine)
  • Oliguria (low urine output <400 ml/day)
46
Q

Symptoms and signs of nephrotic syndrome?

A
  • Proteinuria
  • Oedema
  • Dyslipidemia, lipiduria
  • Hypoalbuminemia
47
Q

What happens to phosphate levels in CKD?

A

Rise as the kidneys cannot remove excess phosphate which leads to PTH release which leads to low blood calcium levels

High phosphate -> low calcium (in blood)

48
Q

Causes of nephritic syndrome

A

Nephritic syndrome is caused by inflammation of glomerulus, and has urine waste; furthermore the cause can be infectious, autoimmune, or thrombotic.[1] The causes can be divided between age groups as:[2]

Children/adolescents

IgA nephropathy
Post-streptococcal glomerulonephritis
Hemolytic uremic syndrome
Henoch–Schönlein purpura
Adults

Goodpasture syndrome
SLE
Rapidly progressing glomerulonephritis
Infective endocarditis

49
Q

Causes of nephrotic syndrome

A

Nephrotic syndrome has many causes and may either be the result of a glomerular disease that can be either limited to the kidney, called primary nephrotic syndrome (primary glomerulonephrosis), or a condition that affects the kidney and other parts of the body, called secondary nephrotic syndrome.

50
Q

What is specific gravity on urine dipstick?

A

To put it another way, the specific density of water would be 1.000.

Ideally, urine specific gravity results will fall between 1.002 and 1.030 if your kidneys are functioning normally.

Specific gravity results above 1.010 can indicate mild dehydration.

The higher the number, the more dehydrated you may be.

51
Q

Primary causes of glomerulonephrosis

A

Primary glomerulonephrosis: Primary causes of nephrotic syndrome are usually described by their histology:

  • Minimal change disease (MCD): is the most common cause of nephrotic syndrome in children. It owes its name to the fact that the nephrons appear normal when viewed with an optical microscope as the lesions are only visible using an electron microscope. Another symptom is a pronounced proteinuria.
  • Focal segmental glomerulosclerosis (FSGS): is the most common cause of nephrotic syndrome in adults. It is characterized by the appearance of tissue scarring in the glomeruli. The term focal is used as some of the glomeruli have scars, while others appear intact; the term segmental refers to the fact that only part of the glomerulus suffers the damage.
  • Membranous glomerulonephritis (MGN): The inflammation of the glomerular membrane causes increased leaking in the kidney. It is not clear why this condition develops in most people, although an autoimmune mechanism is suspected.
  • Membranoproliferative glomerulonephritis (MPGN): is the inflammation of the glomeruli along with the deposit of antibodies in their membranes, which makes filtration difficult.
  • Rapidly progressive glomerulonephritis (RPGN): (Usually presents as a nephritic syndrome) A patient’s glomeruli are present in a crescent moon shape. It is characterized clinically by a rapid decrease in the glomerular filtration rate (GFR) by at least 50% over a short period, usually from a few days to 3 months.

They are considered to be “diagnoses of exclusion”, i.e. they are diagnosed only after secondary causes have been excluded.

52
Q

Secondary causes of glomerulonephrosis

A

Secondary glomerulonephrosis

  • Secondary causes of nephrotic syndrome have the same histologic patterns as the primary causes, though they may exhibit some difference suggesting a secondary cause, such as inclusion bodies. They are usually described by the underlying cause.
  • Diabetic nephropathy: is a complication that occurs in some diabetics. Excess blood sugar accumulates in the kidney causing them to become inflamed and unable to carry out their normal function. This leads to the leakage of proteins into the urine.
  • Systemic lupus erythematosus: this autoimmune disease can affect a number of organs, among them the kidney, due to the deposit of immuno-complexes that are typical to this disease. The disease can also cause lupus nephritis.
  • Sarcoidosis: This disease does not usually affect the kidney but, on occasions, the accumulation of inflammatory granulomas (collection of immune cells) in the glomeruli can lead to nephrotic syndrome.
  • Syphilis: kidney damage can occur during the secondary stage of this disease (between 2 and 8 weeks from onset).
  • Hepatitis B: certain antigens present during hepatitis can accumulate in the kidneys and damage them.
    Sjögren’s syndrome: this autoimmune disease causes the deposit of immunocomplexes in the glomeruli, causing them to become inflamed, this is the same mechanism as occurs in systemic lupus erythematosus.
  • HIV: the virus’s antigens provoke an obstruction in the glomerular capillary’s lumen that alters normal kidney function.
  • Amyloidosis: the deposit of amyloid substances (proteins with anomalous structures) in the glomeruli modifying their shape and function.
  • Multiple myeloma: renal impairment is caused by the accumulation and precipitation of light chains, which form casts in the distal tubules, resulting in renal obstruction. In addition, myeloma light chains are also directly toxic on proximal renal tubules, further adding to renal dysfunction.
  • Vasculitis: inflammation of the blood vessels at a glomerular level impedes the normal blood flow and damages the kidney.
  • Cancer: as happens in myeloma, the invasion of the glomeruli by cancerous cells disturbs their normal functioning.
  • Genetic disorders: congenital nephrotic syndrome is a rare genetic disorder in which the protein nephrin, a component of the glomerular filtration barrier, is altered.
  • Drugs ( e.g. gold salts, penicillin, captopril):[23] gold salts can cause a more or less important loss of proteins in urine as a consequence of metal accumulation. Penicillin is nephrotoxic in patients with kidney failure and captopril can aggravate proteinuria.
53
Q

Cytochrome P450 inducers

Mnemonic: CRAP GPS

A
  • Carbamazepines
  • Rifampicin
  • Alcohol (chronic)
  • Phenytoin
  • Griseofulvin
  • Phenobarbitone
  • Sulphonylureas
54
Q

Cytochrome P450 inhibitors

Mnemonic: SICKFACES.COM

A
  • Sodium valproate
  • Isoniazid
  • Cimetidine
  • Ketoconazole
  • Fluconazole
  • Alcohol (acute)
  • Chloramphenicol
  • Erythromycin
  • Sulfonamides
  • Ciprofloxacin
  • Omeprazole
  • Metronidazole
  • Grapefruit juice
55
Q

What is cytochrome P450 3A4 responsible for metabolising?

A

Calcium channel blockers

Benzodiazepines

HIV protease inhibitors

HMG-CoA-reductase inhibitors

Ciclosporin

Non-sedating antihistamines

56
Q

Cytochrome P450 3A4 inducers and inhibitors.

A

Inducers:

  • Carbamazepine
  • Rifampicin
  • Rifabutin
  • St. John’s wort

Inhibitors:

  • Fluconazole
  • Clarithromycin
  • Erythromycin
  • Grapefruit juice
  • Ritonavir
57
Q

Amiodarone + warfarin drug interaction?

A

The combination of amiodarone and warfarin potentiates the effect of warfarin and prolongs the International Normalized Ratio (INR), increasing the risk of bleeding.

Warfarin is metabolised by CYP2C9.

CYP2C9 is inhibited by:

  • Fluconazole
  • Trimethoprim
  • Amiodarone
  • Zafirlukast
58
Q

What does CKD do to PTH, vitamin D, phosphate and calcium levels in blood?

A
  • Elevated fibroblast growth factor-23 (FGF23)
  • Elevated parathyroid hormone (PTH)
  • Decreased 1,25-dihydroxyvitamin D (1,25D)
  • Elevated serum phosphate
  • Decreased serum calcium.
59
Q

Lower urinary tract is innervated by 3 sets of peripheral nerves involving the parasympathetic, sympathetic, and somatic nervous systems.

Name these.

A

Pelvic parasympathetic nerves: arise at the sacral level of the spinal cord, excite the bladder, and relax the urethra

Lumbar sympathetic nerves: inhibit the bladder body and excite the bladder base and urethra

Pudendal nerves: excite the external urethral sphincter

  • Lumbar sympathetic and voluntary sympathetic nerves prevent one from urinating. Whilst the pelvic parasympathetic nerves cause urination.

A (22 decks)

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