PBL Learning Objectives Flashcards

Question

Foetal membranes and placental structure and function (7.3) - Draw the structure of the placenta

Answer 1

**Feotal membranes:** Amniotic membrane is closest to the foetus (foetal side), chorionic membrane is the maternal side. The membranes 'fuse'. * Amniotic membrane is associated with the amniotic cavity **Placental structure** **Placenta function:** * Delivery of nutrients and gaseous exchange (via maternal-foetal circulation) to the foetus * Removal of waste products *

Answer 2

**Uterine structure:** * Columnar epithelium * Endothelial layer: Formed from the decidua basalis and functionalis layers * Myometrial layer: A thick layer of smooth muscle. 3 layers: Outer longitudinal, middle circular and inner longitudinal **Changes to uterus structure in pregnancy:** * Hypertrophy and hyperplasia of the myometrium * Implantation of the placenta, in the endometrial lining * Uterus undergoes involution (mediated by oxytocin) in puerperium **Function of the uterus in pregnancy** * Contraction (mediated by oxytocin) of the uterus allows for progression of the baby out of the uterus * Expands to accomodate the baby * Attachment site for the placenta

Answer 3

**Causes of bleeding in early pregnancy: (first trimester, 0 -12 weeks)** * Implantation * Miscarriage * Cervical changes * Ectopic pregnancy * Infection * Molar pregnancy: 'Implantation' and growth of abnormal cells within the uterus **Causes of bleeding in late pregnancy:** * Cervical changes - particularly after sex * Vaginal infection * 'Show' * Placental abruption * Placenta praevia: Low lying placenta * Vasa praevia: Foetal placenta vessels lying over the cervix * Uterine abruption: Increased risk following previous C-section * Placenta accreta: Placenta 'invades' too deep into the uterine wall and into the myometrium - becoming inseparable from the uterine wall.

Answer 4

Chorionic villi are seen close to the foetus. Stem villi are seen close to the maternal side of the placenta. The umbilical cord contains 1 umbilical vein and 2 umbilical arteries. Maternal cotyledon: Bulging villous areas. Covered with shreds of decidua basalis

Answer 5

Oestrogen promotes breast tissue development. Progesterone promotes duct development whilst oestrogen promotes breast alveolar development. **Neonatal suckling stimulates release of:** **Prolactin (APG)** (inhibited by oestrogen and progesterone during pregnancy) stimulates the production of milk by the breast lactocytes. **Oxytocin (PPG)** stimulates the contraction of myoepithelial cells. This causes increased intramammary pressure and the 'ejection' of breast milk - milk ejection reflex.

Answer 6

Rhesus disease results from maternal RhD negative blood and foetal RhD positive blood. Testing for RhD Igs is performed. If positive then anti-D immunoglobulin cn be administered, to neutralise the antibodies produced against the Rhesus positive blood. Calls for increased frequency of monitoring during pregnancy.

Answer 7

* Support and advice during pregnancy * Support during labour: Promoting a 'normal' delivery; detecting abnormalities; * Support during the first few weeks after labour, whilst the family adjust to having a baby (postpartum period)

Answer 8

* Abortion may be carried out up to a foetal age of 24 weeks * This causes concern as babies born at 20 weeks have been 'viable' * Can be carried out after 24 weeks if the mothers life if at risk or the baby would be born with a severe disabilty * The unborn child is not protected by the human rights acts

Answer 9

http://www.pathophys.org/uti/

Answer 10

**Definition:** An abrupt deterioration in kidney function, usually over hours or days. It is *usually* reversible over days or weeks. * May cause serious and life-threatening biochemical disturbances that create a medical emergency * CKD is used to define longstanding (\> 3 months), potentially progressive, impairment in kidney function **Clinical features:** Oliguria and rising serum creatinine and/or urea (NOTE urea and creatinine can also be affected by other factors and hence are not always accurate predictors of decreasing renal function) **Causes:** **Pre-renal:** Reduced kidney perfusion causes a reduction in GFR Examples: Hypovolaemia (dehydration, haemorrhage), hypotension, low CO, combinations of the previous examples **Renal:** Parenchymal disorders (damage to the glomerulus, tubule or vessels) **Post-renal:** Urinary tract obstruction, preventing renal excretion of urine.

Answer 11

**Anatomy of the posterior abdominal wall:** Formed from the psoas major, erector spinae and quadratus lumborum muscle. Genitofemoral nerve. Posterior aspect of the diaphragm. Thoracolumbar fascia.

Answer 12

In women: First line: Nitrofurantoin (BID, 5 days) or trimethoprim/sulfamethoxazole (BID, 3 days) Second line: Fosfomycin (single dose)

Answer 13

**Autoregulation:** Independent of hormonal/neural input * **Myogenic reflex:** Smooth muscle response to changes in tubular flow. Increased blood flow increases pressure on the vessel wall, prompts smooth muscle constriction * **Tubuloglomerular reflex:** Macula densa cells detect NaCl flow through the tubule. In response to increased NaCl (caused by increased blood pressure → increased GFR) the cells prompt vasocontriction of the afferent arteriole to slow GFR - creating more 'time' for NaCl reabsorption, **Sympathetic input** * Increases GFR through afferent dilation and efferent dilation **Hormonal/mediator input** * ANP/BNP/ADH * Prostaglandins

Answer 14

* Regulation of ECF and plasma volume * Regulation of osmolality * Endocrine: Synthesis of active vitamin D, synthesis of erythropoeitin * Excretion of waste products * Water reabsorption **A WET BED** **A**cid-base maintenance **W**ater balance maintenace **E**lectrolyte balance **T**oxin removal **B**lood pressure regulation **E**ndocrine (erythropoeitin) **D** vitamin metabolism

Answer 15

**Definition:** May be an upper UTI (kidneys and ureter) or lower UTI (bladder and urethra). Inflammation of the urinary tract. UTIs may be complicated - patients with an increased risk of recurring UTI or poor response to treatment. **Aetiology:** Most commonly caused by ascending bacterial infection. E. coli are the most common agent, as they are spread from the anus. **Signs and symptoms:** * Dysuria * Polyuria * Suprapubic pain * Fever * Nausea (with upper UTI) **Pathophysiology:** Bacterial infection causes inflammation of the urinary tract **Risk factors:** * Female * Incontinence * Increasing age * Sexual intercourse * Spermicide use **Investigations:** * Urine dip: Looking for increased nitrite levels (E. coli) and increased leukocytes * Culture and sensitivity for complicated UTI **Treatment:** * Antibiotics: Nitrofuratoin, trimethoprim, fosfomycin * Lifestyle advice: Adequate hydration, urination following sexual intercourse **Epidemiology:** * Very common

Answer 16

Resultant from reduced GFR. Reduced flow through the kidneys means greater time for reabsorption of H₂O meaning reduced urinary output is seen. The body tries to conserve plasma volume through minimising urinary loss of water. * Haemodynamic abnormalities * Tubular occlusion e.g. ATN, BPH, calculus * Urinary retention * Dehydration * Nephrotoxic drugs * May be related to AKI

Answer 17

* Few drugs are purely nephrotoxic but instead cause damag to the renal system if used under certain conditions. * NSAIDs and ACE inhibitors are the amongst the most common precipitants of renal failure * As urine is concentrated the renal tubules are exposed to high concentrations of drugs and metabolites * Renal damage can cause papillary and/or tubular necrosis * NSAIDs inhibit renal prostaglandin synthesis which leads to vasoconstriction and lowers GFR * Drugs which **impair renal function** - should consider withdrawing during AKI: **Contrast media, ACEi, NSAIDs, diuretics, angiotensin II receptor blocker**

Answer 18

Relations of the bladder, kidneys and ureters

Answer 19

Learn to over-ride the reflex to urinate through co-ordination of the 3 systems and increased myelination. Parasympathetic input (T12-L2): Causes contraction of the detrusor muscle and relaxation of the internal urethral sphincter. Sympathetic input (L2-L4): Causes relation of the detrusor muscle (for expansion of regae) and contraction of the internal urethral sphincter Somatic input (pudendal nerve, L2-L4): Causes contraction of the external urethral sphincter **Storage** * Stretch stimulates GVA firing. GVA fibres travel with pelvic splanchnic nerves. Signal via interneurons within the spinal cord. * Promotes sympathetic input - Detrusor muscle relaxation and internal urethral sphincter contraction * Promotes somatic input - External urethral sphincter contraction * Parasympathetic input is blocked **Voiding** When convenient or when GVA firing becomes 'intense' * GVAs travel to the brain. From here neural signals are initiated * Signals from the sympathetic and somatic systems are blocked - allows for relaxation of the external urethral sphincter * Signals to parasympathetic system to allow for detrusor muscle contraction and relaxation of the internal urethral sphincter * Allows for micturition

Answer 20

Reabsorption occurs mainly at the PCT, with 'fine tuning' occuring at the DCT and CD. **PCT:** * Passive reabsorption: Chloide, urea, bicarbonate and water * Active reabsorption: Glucose, amino acids, plasma proteins (pinocyotosis of those which pass through the basement membrane). * First half sees sodium reabsorption coupled to glucose, water, urea etc. * Second half sees sodium reabsorption coupled to chloride **Bicarbonate reabsorption:** PCT and CD

Answer 21

**Function:** * Ultrafiltration of plasma * Passive process reliant on NFP (3 forces). Passes through 3 layers * Control of blood flow through the capillaries via afferent/efferent arterioles

Answer 22

* **Reabsorption:** Movement of substances from the renal tubule to the capillary * **Secretion:** Movement of substance from the capillary (vasa recta/peritubular) to the renal renal tubule. * **Excretion** via urine

Answer 23

Sees the conversion of ammonia to urea. Occurs in the liver. Urea is then eliminated within the urine via renal tubules, sweat and faeces.

Answer 24

**Definition:** Increased plasma potassium levels. Severe hyperkalaemia being define as \> 6.0 mmol/L, moderate 5.0 - 6.0 mmol/L **Aetiology:** * Decreased K⁺ secretion: AKI, CKD, decreased tubular flow, reduction in aldosterone release, renal tubular acidosis, medications * IncreasedK⁺ release: Rhabdomyolysis, Na⁺/K⁺ ATPase failure, cell lysis (burns/trauma), excessive exercise, acidosis, hyperosmolality (e.g. glucose) **Signs and symptoms:** * Bradycardia * Muscle weakness * Urine changes (oliguria) * Respiratory distress * Decreased cardiac contractabilty * ECG changes * Reflexes (hyperreflexia) **Pathophysiology:** - **Risk factors:** * AKI * Medications: Diuretics, NSAIDs, potassium-sparing diuretics, trimethoprim (acts as a K⁺ sparing diuretics) **Investigations:** * U&E * ECG * FBC * Various tests to allow exclusion of certain aetiologies **Treatment:** * Calcium gluconate: Restore relative membrane potential * Insulin and glucose: Cause movement of K⁺ into cells * Resin for the removal of K⁺ ions **Epidemiology:**

Answer 25

**Definition:** Serum sodium level below 135 mmol/L. A disorder of water balance reflected by an excess of total body water relative to electrolytes. **Aetiology:** **Hypovolaemic hyponatraemia:** Decrease in both total body water and sodium levels but total water is repleted in excess of sodium. **Hypervolaemic hyponatraemia:** Associated with inappropriate baroreceptor perception of low intravascular volume causing ADH release. Water and sodium retention result despite overall increases in water and sodium levels. Increase in both total body water and sodium levels, with total body water increased more so. **Euvolaemic hyponatraemia:** Associated with pathological ADH release. Increased total body water with sodium levels remaining constant. **Signs and symptoms:** _Volume depletion:_ Low urine output; weight loss; orthostatic hypotension; decreased JVP; poor skin turgor; dry mucus membranes; absence of axillary sweat _Volume overload:_ Oedema; crackles on lung auscultation; raised JVP; significant weight gain **Pathophysiology:** Sodium homeostasis is maintained by ADH, thirst, kidneys and aldosterone. **Risk factors:** **Investigations:** **Treatment:** **Epidemiology:** Most common electrolyte inbalance seen in clinical practice.

Answer 26

**Definition:** An inherited condition in which the formation of fluid-filled cysts on the kidneys is observed **Aetiology:** Defective calcium transporter **ADPKD:** 2 possible variants * **PKD1:** 85 % of cases, polycystin 1 protein * **PKD2:** 15 % of cases, polycystin 2 protein **ARPKD:** Enlarged echogenic kidneys in the neonatal period **Signs and symptoms:** * Palpable renal/hepatic mass * Hypertension * Renal insufficiency/ESRD * Hernia * Cardiac murmur **Pathophysiology:** Mutations in the polycystin gene, a cation membrane transporter protein, prevent transport of calcium. The transporter is instead secreted in membranous vesicles within the urine Thought that the polycystin protein acts as a mechanosensitive ion channel. **Risk factors:** * FHx **Investigations:** **Treatment:**

Answer 27

**Manifestations:** * **Decreased excretory function:** * Decreased Na⁺ excretion leading to water retention, hypertension and oedema. * K⁺ excretion per nephron must increase to compensate for the lost nephrons. Patients prone to hyperkalaemia * Decreased ammoniagenesis leads to decreased acid excretion and acidosis * Phosphate excretion is preserved until GFR \< 20 ml/min via decreased reabsorption in the PCT * Accumulation of uraemic toxins * **Decreased urine concentrating capacity** * Decreased capacity to produce dilute urine and to excrete water load * Increased solute load in the nephrons → osmotic diuresis * Loss of medullary hypotonicity * Resistance to ADH * Patients prone to dehydration and nocturia * **Decreased synthetic/endocrine function** * Decreased synthesis of active Vitamin D leads to decreased intestinal Ca²⁺ reabsorption. This prompts increased release of PTH, increasing bone resorption. This in turn adds to phosphate levels (hydroxyapatite) * Decreased EPO synthesis leading to normochromic, normocytic anaemia. This is further aggrevated by hepcidin inhibition of ferroportin. * Dyslipidaemia with elevated TGs and cholesterol seen * **Progressive renal damage**

Answer 28

* Hypertension: Due to decreased Na⁺ and H₂O excretion * Heart murmurs * CV complications: LVH, mitral valve prolapse * Haematuria * Recurrent UTIs * Renal calculi * Abdominal/flank pain * Intracranial aneurysm rupture

Answer 29

**Haemodialysis:** Diverts blood into an external machine in which it is filtered, before returning to the body * Prior to the procedure a arteriovenous fistula must be made. Acts to make a strong vessel through the joining of an artery and a vein. * If the above cannot be done a AV graft may instead be performed (plastic tubing connects the 2 vessels). For short term or in emergency situations a neck line may be used **Peritoneal dialysis:** Dialysis fluid is 'pumped' into the abdomen. Acts to draw out waste products from the passing vessels. There are 2 modalities: * **Continuous ambulatory peritoneal dialysis:** Blood is filtered several times throughout the day * **Automated peritoneal dialysis:** Blood is filtered during sleep **Complications:** Fatigue; hypotension; sepsis; muscle cramps; itching; insomnia

Answer 30

* Weight loss and poor appetite * Oedema (ankles, feet and hands) * SoB * Fatigue * Haematuria * Nocturia * Insomnia * Pruritus * Muscles * Nausea * Impotence

Answer 31

Renal disease symptoms appear when 50 % of nephrons are lost. Hypertension, proteinuria, glomerulosclerosis and progressive loss of nephrons seen. Assessment of **eGFR:** **S****tage 1 (G1)** – a normal eGFR (above 90ml/min), but other tests have detected signs of kidney damage **stage 2 (G2)** – a slightly reduced eGFR (60-89ml/min), with other signs of kidney damage **stage 3a (G3a)** – an eGFR of 45-59ml/min **stage 3b (G3b)** – an eGFR of 30-44ml/min **stage 4 (G4**) – an eGFR of 15-29ml/min **stage 5 (G5)** – an eGFR below 15ml/min, meaning the kidneys have lost almost all of their function KDIGO plots eGFR against **proteinuria:** **A1** – an ACR of less than 3mg/mmol **A2** – an ACR of 3-30mg/mmol **A3** – an ACR of more than 30mg/mmol May progress to ESKD.

Answer 32

* Hypertension * Diabetes * High cholesterol * Glomerulonephritis * Polycytsic kidney disease * Urinary obstruction (calculus) * SLE * Long term use of certain medications

PBL Learning Objectives Flashcards

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