Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 1 > SUGER > Flashcards

SUGER Flashcards

1
Q

What are the 7 functions of the kidney?

A
  1. Waste product removal
  2. Excess fluid removal
  3. Balance salt, water, pH
  4. Control blood pressure
  5. Red blood cell production
  6. Healthy bone maintenance
  7. Removal of drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is total cardiac output, renal blood flow and urine flow rate?

A

Cardiac output - 5L/min
Renal blood flow - 1L/min
Urine flow - 1mL/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Label the blood flow of the kidneys up to efferent arteriole:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Label the blood flow in the kidney after glomerular capillary:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What makes up the juxtaglomerular apparatus and where is it?

A

-Juxtoglomerular cells + macula densa
-It is a modified muscular layer of afferent arteriole in hillum of every glomerulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is there an increased number of in the juxtaglomerular apparatus and what is special about them?

A

-Increased number of smooth muscle cells
-Thicker cells
-Less actin/mysoin but many granules containing renin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What do juxtaglomerular cells and macula densa do?

A

-Act as barometers to changes in BP
-LOW BP = LESS DISTENDED WALLS = RENIN RELEASE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What kind of regulation is seen by the kidney in terms of its rate of processes?

A

-Autoregulation = intrinsic
-Maintains constant GFR (Glomerular Filtrate Rate) and excretion of water and waste products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What two mechanisms are involved in the auto regulation of the kidney?

A

-Tubuloglomerular feedback
-Myogenic mechanism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Label the tuboglomerular regulation in the kidney:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What system does renal perfusion from the tuboglomerular autoregulation afffect?

A

RAAS system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the myogenic autoregulation in the kidneys:

A

-Decrease in BP does opposite
-ONLY PRE_GLOMERULAR RESISTANCE VESSELS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What happens at the filtration barrier at the glomerulus?

A

Passage of fluid from the blood into Bowman space to form filtrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the distal part of the nephron responsible for?

A

Secretion and reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Label this diagram of the renal filtration barrier:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the 3 components of the renal filtration barrier?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Label this bit of the kidney:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What 5 factors determine filtration in the kidney?

A

-Pressure
-Size of molecule
-Charge
-Rate of blood flow
-Protein binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What forces favour and oppose filtration in the kidney?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How does size affect filtration in the kidney?

A

-Small molecules and ions up to 10kDa can pass freely e.g. glucose, uric acid, potassium, creatinine
-Large molecules increasingly restricted e.b. plasma proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How does charge affect filtration in the kidneys?

A

-Fixed negative charge in GBM (glomerular basement membrane) (glycoproteins) repel negatively charged anions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How does rate of blood flow affect kidney filtration?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How does protein binding affect filtration in the kidney?

A

-Albumin has molecular weight of around 66kDa but is -ve so cannot easily pass through
-Filtered fluid is essentially protein free
-Tamm Horsfall protein in urine produced by tubule
-Affects drugs, calcium, thyroxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What can damage to the kidney filtration barrier cause?

A

-Protein leak called nephrotic syndrome
-Immune conditions/genetic abnormalities
-Diabetes damages filtration barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the basic glomerular filtration rate equation?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the more complicated glomerular filtration rate equation?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is glomerular filtration rate determined by (3)?

A

-Net filtration pressure
-Permeability of the filtration barrier
-Surface area available for filtration (approx 1.2-1.5m2 total

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What two external things regulate the glomerular filtration rate?

A

-Sympathetic nervous system
-Hormones/autocoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the innervation to afferent and efferent arterioles and their consequence?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What 6 hormones affect GFR?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

how do each of these hormones affect GFR?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What two changes to afferent and efferent arterioles can increase GFR?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What two changes to afferent and efferent arterioles can decrease GFR?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Is GFR measured directly?

A

-NO
-Calculated using excretion marker (M)
-Usually creatinine (muscle metabolite and constantly produced)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the GFR indirect equation?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Properties of a good urine marker?

A

-Freely filtered
-Not secreted or absorbed
-Not metabolised
-ALL M FILTERED WILL END UP IN THE URINE, NO MORE AND NO LESS AS IT ISN’T SECRETED OR REABSORBED

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Normal GFR?

A

125mL/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What things can affect creatinine?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the gold standard marker for measuring GFR?

A

-Inulin
-Not very easily carried out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What terms are used for high and low blood pH?

A

Acidemia = low blood pH
Alkalemia = High blood pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Label the main pH balance systems:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are pH and HCo3- governed by?

A

pH and HCO3- are dependant variables governed by:
-pCO2
-Conc of weak acids(ATOT)
-Strong ion difference (SID)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the general Henderson-Hasselbach equation?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the Henderson-Hasselbach equation relating to acidosis?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What 6 things do we measure in relation to acidosis (ABG)?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is the standard bicarbonate?

A

-Bicarbonate concentration standardised pCO2 5.3kPa and temp 37
-Measure of metabolic component of any acid-base disturbance
-“What would the bicarbonate be if the CO2 was normal?”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is absolute bicarbonate affected by?

A

Respiratory and metabolic components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is base excess?

A

-Quantity of acid required to return pH to normal under standard conditions
-Can be used to calculate bicarbonate dose to correct acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What value does base excess have in what conditions?

A

Negative in acidosis, can be referred to as base deficit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What can acid-base disorders be classed into?

A

-Acidoses and alkaloses
-Respiratory (CO2 excretion change) or metabolic (changes in acid load, excretion or bicarbonate recycling)
-Can co-exist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are clinical features of metabolic acidosis?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the anion gap?

A

-Difference between measured anions and cations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What three things can cause metabolic alkalosis?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is the compensatory mechanism for metabolic alkalosis?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the mechanism of respiratory acidosis?

A

CO2 retention, leading to increased carbonic acid dissociation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What causes respiratory acidosis?

A

-Any cause of respiratory failure
-Comp mech – increased renal H+ excretion and bicarbonate retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the mechanism of respiratory alkalosis?

A

CO2 depletion due to hyperventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the causes and compensation for respiratory alkalosis?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What questions are asked in a ABG interpretation?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Describe the proximal tubule cells and their processes:

A

-Active reabsorption of multiple solutes
-Metabolically active cells – lots of mitochondria
-Sodium gradient generated by Na/K ATPase
-Vulnerabe to hypoxia and toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is glycosuria?

A

-Defect in sodium glucose transporter 2 (SGLT2)
-Mechanism – failure of glucose reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is cystinuria?

A

-Defect in renal basic amino acid transporter (rBAT)
-Mechanism – failure of cystine reabsorption, increased urinary cystine conc (stone formation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Label this diagram of bicarbonate reabsorption:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is proximal renal tubular acidosis?

A

Defect in Na/H antiporter
Mechanism – failure of bicarbonate reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What does the Loop of Henle do?

A

-Generates medullary concentration gradient
-Active Na reabsorption in thick ascending limb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What are the basic ion movements in the ascending limb?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What do the distal tubule and collecting duct do?

A

-Distal tubule and cortical collecting duct allow “fine tuning” of sodium reabsorption, potassium and acid-base balance
-Collecting duct mediates water reabsorption and urine concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is the action of aldosterone?

A

-Steroid hormone
-Increases expression of ENaC and Na/K ATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is distal (Type 1) renal tubular acidosis?

A

Defect in luminal H+ ATPase or H+/k+ ATPase
Mechanism – faliure of H+ excretion and urinary acidification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is distal (Type 1) renal tubular acidosis?

A

Defect in luminal H+ ATPase or H+/k+ ATPase
Mechanism – faliure of H+ excretion and urinary acidification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What does excessive aldosterone activity produce?

A

-Sodium retention
-Hypertension
-Hypokalaemic alkalosis
-Can be primary or secondary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the basic embryology of the endocrine pancreas?

A

-Junction of foregut and midgut 2 pancreatic buds generated and fuse to form pancreas
-Exocrine functions begin after birth
-Endocrine function from 10-15 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Describe the basic anatomy of the pancreas:

A

-Retroperitoneal and post to greater curvature of stomach
-12-15cm long, head near C of duodenum
-Secretions pass into small ducts then larger ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What cells is the pancreas formed of?

A

-Formed of small clusters of glandular epithelial cells
-98-99% clusters called acini

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What cells carry out exocrine and endocrine functions of the pancreas?

A

-Exocrine - acinar cells:
-Manufacture and secrete fluid and digestive enzymes (pancreatic juice) released into gut
-Endocrine - islet cells:
-Manufacture and release several peptide hormones into portal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What happens in the islets of langerhans?

A

-Site of insulin and glucagon secretion of the endocrine pancreas
-2-3% of total pancreas volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What islet cells produce what?
What term is used to describe them?

A

-Heterogeneous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Label these cells to their functions:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Label the functions of each of these cells:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What peptide hormones are produced by the islets and describe them?

A

Insulin
-Polypeptide
-Reduced glucose output by liver
-Increases storage of glucose, FA, AA
Glucagon
-Polypeptide
-Mobilises glucose, FA, AA from stores
Somatostatin
-Inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

How can you describe the actions of insulin and glucagon to each other?

A

Reciprocal actions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are the 3 key functions of insulin?

A

Suppresses hepatic glucose output
- Decrease glycogenolysis and gluconeogenesis
Increase glucose uptake into insulin sensitive tissues
-Muscle - glycogen + protein synth
-Fat - FA synthesis
Supresses
-Lipolysis
-Breakdown of muscle (decreased ketogenesis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What are the 3 key functions of glucagon?

A

It is counter-regulatory to insulin
Increases hepatic glucose output
-Increase glycogenolysis and gluconeogenesis
Reduced peripheral glucose uptake
Stimulates peripheral release of gluconeogenetic precursors (glycerol, AA)
-Lipolysis
-Muscle, glycogenolysis and breakdown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What other things have similar effects to glucagon?

A

-Other counterregulatory hormones
(adrenaline, cortisol, growth hormone
-Become relevant in certain disease states

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

How should glucose levels remain and what is a short term buffer of this?

A

-Should remain constant
-Liver glycogen is a short term glucose buffer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What are the short and long term responses to high blood glucose?

A

Short term - Make glycogen (glycogenesis)
Long term - Make triglyceride (lipogenesis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What are the short and long term responses to low blood glucose?

A

Short term - Split glycogen (glycogenolysis)
Long term - Make glucose from amino acids/lactate (gluconeogenesis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

How is glucose sensed?

A

-Primary glucose sensors in pancreatic islets
-Also in medulla, hypothalamus and carotid bodies
-Inputs from eyes, taste buds, gut all involved in regulating food
-Sensory cells in gut wall also stimulate insulin release from pancreas - incretins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Is insulin response greater following oral or IV glucose and why?

A

-Higher after oral despite similar plasma glucose concentrations
-Gut hormones stimulate insulin release are called incretins - glucagon-like peptide (GLP-1) and glucose-dependant insulinotrophic peptide (GIP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What are 2 features of GLP-1?

A

-Glucose dependant
-Short half life (1-2 mins) - DPP-IV cleaves GLP-1 to prevent hypoglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Describe CHO metabolism in a fasting state:

A

-All glucose comes from liver:
-Glycogenolysis
-Gluconeogenesis (3 carbon precursors such as lactate, alanine, glycerol)
-Glucose delivered to insulin dependant tissues - brain + RBC
-Insulin levels low
-Muscle uses FFA for fuel
-Some processes are very sensitive to insulin, low insulin levels prevent unrestrained breakdown of fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What is the first stage of insulin secretion by the beta cell?

A

-Glucose equilibrates across the plasma membrane via GLUT2 transporters - varies on conc
-Intracellular conc tracks extracellular
-Phosphorylated by glucokinase to G6P
-Glycolysis increases and ATP in generated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What is the second stage of insulin secretion by beta cells?

A

-ATP closes KATP channel and stops the efflux of K+
-Depolarises membrane allowing opening of voltage-dependant Ca2+ channels
-Rapid influx of Ca2+
-Triggers insulin exocytosis from primed secretory granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Describe CHO metabolism after feeding:

A

-Physiological need to dispose of nutrient load
-Rising glucose stimulates 5-10 fold increase in insulin secretion + suppress glucagon
-40% to liver, 60% periphery (muscle)
-Replenished glycogen stores
-Excess converted to fats
-Suppress lipolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What does proinsulin contain?

A

-A and B chains joined by the C peptide
-Disulfide links A + B
-Presence of C peptide implies endogenous insulin production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What kind of release is insulin and what does this mean?

A

-Biphasic
-B-cells sense rising glucose and aim to metabolise it
-First phase response = rapid release of stored product
-Second phase response is slower and is release of newly synthesised hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What is the insulin action in muscle and fat cells?

A

-GLUT4 insulin receptor is a high affinity large transmembrane glycoprotein
-Mechanism not fully understood
-Causes exocytosis of GLUT4 vesicles, increasing glucose transporters in the cell membrane and rapid uptake of glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Describe normal puberty:

A

-Centrally driven
-Depends on intact HPG axis
-Influenced by many other factors
-Trigger is not well understood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What 5 other factors influence normal puberty?

A

-Nutrition
-Leptin and insulin
-Socio-cultural
-Genetic
-Exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What are 3 causes of precocious puberty?

A

-Gonadotrophin dependant (true or central)
-Intracranial lesions, infections, hypothyroidism
-Gonadotrophin independant
-CAH, sec hormone secreting tumours
-Other variants
-Premature thelarche

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What is the treatment for precocious puberty?

A

-Exclude cause
-Do nothing
-Inhibit puberty with GnRH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What are the 3 groups of causes of delayed puberty?

A

-General
-Constitutional delay
-Malabsorption
-Chronic disease
-Gonadal failure
-Turner syndrome
-Gonadotrophin deficiency
-Hypothalamic/pituitary lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What can be some treatment options for delayed puberty?

A

-Exclude physical causes
-Sex hormone treatment
-Growth hormone therapy (occasional)
-Treatment of associated infertility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What is the genetic determinant of sex and its mechanism in males?

A

-SRY gene switches testicular development
-Testes produce MIF
-Prevents Mullerian duct development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What is the genetic determinant of sex and its mechanism in females?

A

-Absence of Y chromosome
-Ovaries and Mullerian ducts form
-Uterus and fallopian tubes form
-Two X chromosomes required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What are the general features of germ cells?

A

-Specialised cells – develop into gametes
-Migration to genital ridge by amoeboid movement
-Rapid mitotic division until about 20 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Describe the replication and numbers of oocytes over what timescale?

A

-5-10 million primary oocytes at 20 weeks
-Meiosis starts before 12 weeks
-Rapid oocyte death at 20 weeks
-1 million left at birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What is the importance of meiosis (4)?

A

-Two meiotic divisions prevent polyploidy
-Key step in germ-cell differentiation
-Increases chromosomal combinations and genetic variability
-Variability contributes to genetic or bio-diversity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Describe meiosis 1 in females:

A

-Reduction division
-46XX = 23X + 23X
-In-utero before 12 weeks
-Homologous recombination & crossover
-Arrested at metaphase 1 until puberty
-Resumption triggered by LH surge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Describe meiosis 2 in females:

A

-Equational division
-23X = 23X + 23X
-Arrested at metaphase 2 until fertilisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Summarise primitive gonads before 6th week:

A

Identical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Summarise primitive gonads after 6 weeks:

A

-If Y chromosome (SRY gene) present:
-Testes form
-Mullerian development inhibited
-If Y chromosome absent:
-Ovaries form
-Mullerian development occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Describe the basic embryology of the female genital tract:

A

-Paramesonephric (Mullerian) duct develops:
-Fallopian tubes
-Uterus
-Upper 2/3 of vagina
-Mesonephric regresses
-Lower vagina
-Clitoris, labial majora and minora

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Describe the hypothalamic-pituitary-gonadal axis:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

When does positive and negative feedback occur during the hypothalamic-pituitary-gonadal axis during the menstrual cycle?

A

-Positive feedback – days 12-14
-Negative feedback – most of cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What is the hormonal control of puberty before puberty?

A

-Low pulsatility amplitude of GnRH and GnRH secretion from hypothalamus
-Low levels of (pituitary) FSH, LH and (gonadal) sex steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

What is the hormonal control of puberty at pubertal age?

A

-Increased amplitude of GnRH and GHRH
-Increased levels of FSH, LH and sex steroid
-Increased levels of growth hormone (GH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What are the testes covered by anteriorly?

A

-Covered anteriorly by a saclike extension of the peritoneum (tunica vaginalis)
-Descended into the scrotum with the testes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What is the tunica albuginea?

A

White fibrous capsule

136
Q

What do the septa divide in the testes?
What is produced by these structures?

A

Divide organ into compartments containing seminiferous tubules where the sperm are produced

137
Q

What are Leydig cells?

A

Clusters of cells between the seminiferous tubules and source of testosterone

138
Q

What do Sertoli cells do?

A

Promote sperm cell development
Blood-testis barrier is formed by tight junctions between Sertoli cells
Seperating sperm from immune system

139
Q

What do seminiferous tubules drain into?

A

Drain into network called rete testis

140
Q

Describe the histology of the testis:

A
141
Q
A
142
Q
A
143
Q

What does this show?

A

Heat exchange at the pampiniform plexus

144
Q

Describe the stages of meiosis:

A

-Production of gametes haploid cells required for sexual reproduction
-2 cell divisions
-Meiosis 1 = separation of homologous chromosome pairs = 2 haploid cells
-Meisos 2 – separation of sister chromatids = 4 haploid cells

145
Q

Where does meiosis occur in males?

A

Seminiferous tubules of males

146
Q

What does spermatogenesis produce?

A

-2 kinds of daughter cells (spermatogonium)
-Type A remain outside blood-testis barrier & produce more daughter cells until death
-Type B differentiate into primary spermatocytes

147
Q

Describe the movement of type B spermatogonium:

A

-Must pass through BTB to move inward toward lumen – new tight junctions form behind these cells
-Meisosi I -> 2 secondary spernatocytes
-Meiosis II -> 4 spermatids

148
Q

What transformation occurs in spermiogenesis?

A

-Transformation of spermatids into spermatozoa
-Sprouts tail and discards cytoplasm to become lighter

149
Q
A
150
Q

What is the rate of production of sperm?

A

300 to 600 sperm are made per gram of testis per second

151
Q

What forms the blood-testis barrier?

A

Tight junctions between and basement membrane under Sertoli cells

152
Q
A
153
Q

What occurs during spermiogenesis?

A

-Changes that transform spermatids into spermatozoa
-Discarding excess cytoplasm and growing tails

154
Q

Label this diagram:
What is the process?

A

Spermiogenesis

155
Q

Label this diagram:
What process does it show?

A

Feedback control of the hypothalamus-pituitary-testicular axis

156
Q

Describe the head of the spermatazoon:

A

-Head is pear-shaped front end
-Contains nucleus, acrosome and basal body of the tail flagellum
-Nucleus = haploid chromosomes
-Acrosome = enzymes to penetrate egg
-Basal body

157
Q

Label:
What is it?

A

Spermatazoon

158
Q

Describe the tail of the spermatazoon:

A

Divided into 3 regions:
-Midpiece contains mitochondria around axoneme of flagellum (ATP for movement)
-Principal piece is axoneme surrounded by fibres
-Endpiece is axoneme only and is very narrow tip of flagellum

159
Q

What are the 4 spermatic ducts?

A

-Efferent ductules
-Epididymis
-Ductus (vas) deferens
-Ejaculatory duct

160
Q

Describe the efferent ductules and epididymis:

A

Efferent ductules:
-12 small ciliated ducts collecting sperm from rete testes and transporting to epididymis
Epididymis:
-Coiled duct adhering to posterior testis
-Site of sperm maturation and storage

161
Q

Describe the ductus (vas) deferens and ejaculatory duct:

A

Ductus (vas deferens):
-Muscular tube passing up from scrotum through inguinal canal to posterior bladder surface
-Widens into terminal ampulla
Ejaculatory duct:
-Forms from vas deferens & seminal vesicles passing through prostate to empty into urethra

162
Q
A
163
Q

What are the three accessory glands of sperm production?

A

-Seminal vesicles
-Prostate gland
-Bulbourethral glands

164
Q

What volume os seminal fluid is expelled during orgasm and what is it made of?

A

-2-5mL of fluid expelled
-60% seminal vesicle fluid
-30% prostatic
-10% sperm
-Trace of bulbourethral fluid

165
Q

What is normal sperm count and what are sperm’s main function?

A

-50-120 million/mL
-Serve to digest path through cervical mucus and to fertilize egg

166
Q

What are some other components of semen?

A

-Fructose for energy for sperm motility
-Fibrinogen

167
Q

What happens to the fibrin in the semen?

A

-Clotting enzymes convert fibrinogen to fibrin causing semen to clot
-Fibrinolysis liquefies semen within 30 mins
-Prostaglandins stimulate female peristaltic contractions

168
Q

Describe oocyte activation (Day 1):

A

-First stage
-Sperm protein called Phospholipase C zeta (PLCz)
-Activates the egg to release calcium from internal stores
-Activation is essential for the transformation of the decondensed sperm nucleus in to pronucleus

169
Q

What happens 4-7 hours after gamete fusion?

A

-Two sets of haploid chromosomes form the female and male pronucleus (23 chromosomes each)
-Pronuclei are equal in size and contain nucleoli
-In IVF multinucleate oocytes can be identified - polyspermic

170
Q

Describe syngamy:

A

-Male and female pronucleus migrate to centre (cytoskeleton role)
-Haploid chromosomes pair and replicate DNA prepping for first mitosis
-Pronuclear membranes break down
-Mitotic metaphase spindle forms
-46 chromosomes organise at spindle equator

171
Q

Describe day 2 of embryo development:

A

-Cleavage
-Approx 24 hours post-fertilisation ooplasm divides into two equal halves
-If one or more of the PN fail to decondense and move in to one of blastomeres, diploid or triploid mosaics may occur

172
Q
A
173
Q

What are cleavages during embryonic development controlled by?

A

-Timed from sperm entry by oocyte program that also regulates ‘house keeping’ in embryo
-Successive cleavages result in an increase in cell no. - essential to have enough for differentiation

174
Q

Prior to 4-8 cell stage of embryo development, what does control depend on?

A

-Depends on maternally-derived stores of RNA laid down during oogenesis
-Activation of the embryonic genome and start of embryonic transcription occurs in a 4-8 cell embryo
-Arrest can occur

175
Q

How do you describe early cleavage stage embryos?

A

-Totipotent
-Nuclei of individual blastomeres are each capable of forming an entire foetus

176
Q

describe the 5th day of embryo development:

A

-Cavitation and differentiation
-Tight junctions between outer cells - trophectoderm
-Fluid-filled cavity expands
- >80 cells
- 55-66% comprise trophectoderm rect is ICM
-Pluripotent

177
Q
A
178
Q

What do the trophectoderm cells do?

A

Pump fluid to the embryo to form the blastocoel cavity

179
Q

Describe day 5/6 of embryo development:

A

-Expansion
-Cavity expands
-Diameter increases
-ZP thins

180
Q

Describe day 6+ of embryo development:

A

-Hatching
-Blastocyst expansion and enzymatic factors cause the embryo to hatch from the ZP
-Needed for implantation
-TE - extraembryonic
-ICM - embryonic

181
Q

Describe the basics of the first 6 days of embryonic development based on the diagram:

A
182
Q

What is the energy metabolism of the early preimplantation embryo?

A

-ATP turnover low
-ATP/ADP high
-Energy metabolism = consumption of pyruvate
-Glucose uptake + utilisation low

183
Q

What are the energy metabolism and requirements at the blastocyst stage?

A

-Metabolic activity rises sharply
-ATP/ADP falls reflecting an increase in energy demand -> protein synth and ion pumping
-Glucose is predominant exogenous energy substrate

184
Q

Label:

A
185
Q
A
186
Q

What is the provision of exogenous nutrients in vivo?

A

Supplied by:
-Cumulus cells
-Fallopian tube secretions
-Uterine secretions (iron and fat-soluble vitamins)

187
Q

What exogenous nutrients are present in vivo of the embryo and how do they differ?

A

-Concentrations of nutrients vary along the tract to provide the embryo requirements
-Growth factors and cytokines

188
Q

What happens at 10 days of embryo development?

A

-Cellular differentiation
-After implantation, embryogenesis continues with the next stage of gastrulation when 3 layers of germ cell develop (histogenesis)
-Three layers formed
-All structures of body are derived from these structures

189
Q

What forms the chorion and placenta?

A

-Chrorioic ectoderm (trophectoderm)
-Extra embryonic mesoderm (icm)

190
Q

What forms the amnion and yolk sac?

A

Extra embryonic membrane, mesoderm and endoderm

191
Q

What forms the fetus?

A

Embryonic ectoderm, mesoderm and endoderm

192
Q

What are 3 statements about the embryo implantation process?

A

-Well defined starting point
-Gradual process over several weeks
-No agreement of when complete

193
Q

What does this show?

A

-1 day after initiation of implantation
-Note the small size of implantation compared to the thickness of the endometrium

194
Q

Describe the regulation of the implantation process of the embryo:

A

-After embryo hatched embryonic and maternal cells enter complex dialogue
-High degree of prep and coordination
-Controlled cascade of trophoblast proliferation, differentiation, migration and invasion

195
Q

What mechanisms are involved in the embryo implantation? (5)

A

-Hormones (sex steroids)
-Cell adhesion molecules
-Proteases
-Cytokines, growth factors
-Genetic

196
Q

What are the 3 phases of embryo implantation?

A

-Apposition
-Attachment
-Invasion

197
Q

Describe apposition:

A

-Unstable adhesion of blastocyst to uterine lining
-Synchronisation of embryo + endometrium
-Hatched blastocyst orientates via embryonic pole
-Receptive endometrium (window day 19-22)

198
Q

Describe attachment (adhesion):

A

-Stronger adhesion
-Penetrates with protrusions of trophoblast
-Massive communication via ligand-receptor interactions
-Integrin subunits (endometrial)
-integrins (trophoblasts)
-Briding ligands connect integrins

199
Q

Describe invasion (penetration):

A

-trophoblast protrusions continue to proliferate and penetrate endometrium
-Cells change to syncytiotrophoblast
-highly invasive - expands + erodes endometrial stroma)
-Erodes endometrial blood vessels
-Comes into contact with maternal blood to form chorionic villi - initiation of placenta formation
-Blood filled lacunae form

200
Q

Describe the decidual reaction:

A

-Progesterone promed endometrial stromal cells next to blastocyst differentiate into metabolically active decidual cells (secratory)
-Endometrial glands enlarge
-Local uterine wall becomes highly vascularised
-Secretions -> growth factors, other nutrients to support growth

201
Q

What are the main roles of progesterone (embryo development)?

A

-Modifies distribution of oestrogen receptors
-Stimulates secretory activity
-Stimulates stromal oedema
-Increase volume of blood vessels
-Primes decidual cells

202
Q

What is maternal recognition of the embryo?

A

-Embryo is antigenically different from the mother
-At the same time as the decidual reaction, leucocytes in endometrial stroma secrete interleukin-2
-Prevents maternal recognition of embryo as a foreign body

203
Q

What is the role of hCG?

A

-Essential to sustain early pregnancy
-Ensures corpus luteum continues to produce progesterone throughout first trimester of pregnancy (prevent menstruation)
-Interacts with endometrium via specific receptors
-immunosuppressive - highly negative charge to repel immune cells from fetus

204
Q

Where is hCG produced?

A

Produced in the human placenta by the synctiotrophoblast

205
Q

Describe the hCG measurement in early pregnancy:

A

-Doubling time of hCG is 1.3 days in the first 10-12 days of pregnancy
-Short doubling time signifies healthy pregnancy

206
Q

What things are generated that need to be excreted by the kidney?

A

-Volatile acids from diet (sulphuric)and protein metabolism (phorphoric)
-Lactate from anaerobic metabolism
-Volatile acid co2 from carb metab

207
Q

What do the kidneys excrete and reclaim?

A

-Excrete the acid load and reclaim filtered bicarboante

208
Q

Describe the excretion of H+ ions in the ascending tubule:

A
209
Q

Describe the reclaim of filtered bicarbonate in the kidney:

A
210
Q

Describe metabolic acidosis:

A

-Low arterial pH
-Conjunction with a reduced serum HCO3- conc

211
Q

Describe metabolic alkalosis:

A

-Caused by retention of excess alkali and manifested by an increase in venous (total Co2) or arterial HCO2-

212
Q

Describe respiratory acidosis:

A

Acid-base disturbance initiated by an increase in CO2 tensions of body fluids and whole body CO2
-Secondary increment in plasma bicarbonate observed in acute and chronic hypercapnia is integral part

213
Q

Describe respiratory alkalosis:

A

-Reduction in CO2 tension of body fluids
-Secondary decrease in HCO3- observed in acute and chronic hypocapnia is integral part

214
Q

Label this diagram of the compensations in acid-base disorders:

A
215
Q

What 2 basic things are needed for normal lower urinary tract function?

A

-Urine storgae - low pressure with perfect continence
-Urine emptying - periodic complete urine expulsion at low pressure when convenient

216
Q

Describe the two basic phases of micturition and what occurs during each:

A
217
Q

Describe the neural control of micturition throughout life:

A

Non potty trained baby = coordinated voiding + no control of off to on

Neurologically normal adult = coordinated voiding + full control when switches from off to on

Old age = same as non-potty trained

218
Q

What are the 4 nerves of the lower urinary tract?

A

Motor:
-Pelvic
-Hypogastric
-Pudendal
Sensory:
-Visceral afferents

219
Q

Describe the pelvic nerve:

A

-Autonomic/Parasympathetic
-S2-S4 intermediolateral horn (sacral micturition centre)
-Bladder contraction

220
Q

Describe the hypogastric nerve:

A

-Autonomic/Sympathetic
-T10-L2 intermediate horn
-Bladder relaxation/bladder neck contraction

221
Q

Describe the hypogastric nerve:

A

-Autonomic/Sympathetic
-T10-L2 intermediate horn
-Bladder relaxation/bladder neck contraction

222
Q

Describe the pudendal nerve:

A

-Somatic (voluntary)
-S2-S4 ventral horn
-Striated external sphincter and pelvic floor contraction

223
Q

Describe the visceral afferents of the urinary tract:

A

-Sensory autonomic
-S2-S4 intermediolateral horn (sacral micturition centre)
-A-delta bladder stretch, C-fibres pain

224
Q

Label the red:

A
225
Q

Label the green:

A
226
Q

Label the green:
Bladder filling control

A
227
Q

Label the blue:
Bladder filling control

A
228
Q

Label the blue:
Bladder emptying stage

A
229
Q

Label the purple:
Bladder emptying stage

A
230
Q

Describe the bladder storage reflex:

A

-Distention of the bladder produces low-level bladder afferent firing
-Triggers guarding reflex
-sympathetic outflow via hypogastric to bladder outlet
-pudendal outflow to external urethral sphincter
-Sympathetic outflow also inhibits contraction of detrusor muscle
A REGION IN ROSTRAL PONTINE STORAGE CENTRE MIGHT INCREASE STRIATED URETHRAL SPHINCTER ACTIVITY

231
Q

Label this diagram of the bladder storage reflex:

A
232
Q

Describe the voiding reflex:

A

-Intense bladder-afferent firing in pelvic nerve
-Triggers spinobulbospinal reflex:
-Afferent signals passed to periacqueductal gray (blue)
-Pontine micturition centre activated
-PMC on/off switch
-para outflow to bladder and urehral smooth muscle (green)
-inhibits symp and pudendal outflow to bladder outlet (red)

233
Q

What are the 4 important central neural control mechanisms of micturition?

A

-Prefrontal
-PAG
-PMC
-Basal ganglia

234
Q

What are the prefrontal and PAG actions on micturition?

A
235
Q

What are the PMC and and basal ganglia actions of micturition?

A
236
Q

What are the two classifications of lower urinary tract dysfunction?

A

-Failure to store
-Failure to void

237
Q

What 3 situations lead to a loss of relationship between plasma osmolality and vasopressin?

A

-Drinking rapidly suppresses vasopressin release and thirst
-In pregnancy the osmotic threshold for VP release and thirst is decreased
-Plasma VP concentrations increase with age

238
Q

What are the medical terms for large volumes of urine and drinking?

A

Large volume of urine - polyurea
Large volumes of drinking - polydypsia

239
Q

What 3 things categorise diabetes insipidus?

A

-Polyuria
-Polydypsia
-No glycosuria or hypercalcaemia or hypokalaemia

240
Q

What are the two types of diabetes insipidus?

A

-Cranial - lack of vasopressin
-Nephrogenic - resistance to vasopressin

241
Q

how does the relationship between plasma AVP and plasma osmolality differ with diabetes insipidus?

A
242
Q

What are the two causes of cranial diabetes insipidus?

A

-Destruction of hypothalamus
-interruption of the connection of hypothalamus to pituitary

243
Q

What stimulates the release of oxytocin?

A

Release stimulated by milk suckling
Posterior pituitary

244
Q

What is the action of oxytocin?

A

-Stimulates milk let down
-Stimulates contraction of myometrium
-200 times less active at the V2 receptor compared to AVP

245
Q

Describe the cycle of the release of oxytocin:

A
246
Q

Describe the action of AVP:

A
247
Q
A
248
Q
A
249
Q

What does the posterior pituitary originate from?

A

-Neuro tissue
-Large number of glial-type cells

250
Q

What two hormones are secreted from the posterior pituitary?

A

-Vasopression (ADH) primarily from supraoptic nuclei – control water secretion into urine
-Oxytocin – expression of milk from the glands of the breasts to the nipples (promotes onset of labour) – primarily paraventricular nuclei

251
Q
A
252
Q
A
253
Q

What are the volumes in the body?

A

Total body water = 42L
Intracellular = 28L
Extracellular = 14L – Intravascular =3.5L / Interstitial = 10.5L

254
Q

What is the relationship between plasma osmolality, urine osmolality and plasma vasopressin?

A
255
Q

What are the urine concentrations in the different parts of the nephron?

A
256
Q

What is the mechanism of action of vasopressin? (4 steps)

A
257
Q
A
258
Q

What two things regulate ADH release?

A

-Osmoreceptors
-Baroreceptors

259
Q

What three things affect the release of vasopressin?

A
260
Q
A
261
Q

What does AVP interplay with?

A

There is an interplay between AVP and salt and water physiology with other hormones

262
Q

Describe the AVP control of dehydration:

A
263
Q

What is osmolality?

A

Concentration of particles per kilo of fluid

264
Q

What isn’t important with osmolality?

A

-Size of particle
-Number is important

265
Q

What things can affect osmolality at high enough concentrations?

A

-Sodium
-Potassium
-Chloride
-Bicarbonate
-Urea and glucose

266
Q

What do alcohol, methanol, polyethylene glycol or mannitol do to affect osmolality?

A

All exogenous solutes that may affect osmolality

267
Q

What is normal osmolality?

A

282-295 mOsmol/kg

268
Q

What is the general relationship of pAVP and pOsm?

A

-Past a certain pOsm, pAVP increases directly proportionally

269
Q

What other thing shows a similar relationship to pAVP and pOSm?

A

Thirst

270
Q

What is the general relationship between plasma AVP concentration and urine concentration?

A

Urine osmolality increases with pAVP after a small delay

271
Q

What are the 3 layers of the skin?

A

-Epidermis
-Dermis
-Subcutis

272
Q

What gives skin its waterproof barrier?

A

-Tight junctions between cells in stratum granulosum
-Epidermal lipids
-Keratin in stratum corneum
Form both an inside-out and outside-in waterproof barrier to water

273
Q

What does the waterproof barrier of the skin do?

A

Prevents transepidermal water loss

274
Q
A
275
Q

What are the 6 functions of the epidermis?

A

-Waterproofing
-Physical barrier
-Immune
-Vitamin D synthesis (endocrine)
-UV protection
-Thermoregulation

276
Q

What are the 3 functions of the dermis?

A

-Thermoregulation
-Vitamin D synthesis (endocrine)
-Sensory organ

277
Q

Describe the 5 functions of the subcutis:

A

-Thermoregulation
-Energy reserve
-Vitamin D storage
-Endocrine organ
-Shock absorber

278
Q

Describe skin wrinkling when wet:

A

-Mediated by sympathetic nervous system
-Vasoconstriction in dermis
-Improves grip

279
Q

Describe the skin’s features as a physical barrier:

A

-Structure of skin helps resist trauma
-Stratified epithelium helps resist abrasive forces
-Fat in subcutis acts as shock absorber

280
Q

Describe vitamin D synthesis in the skin:

A

-7-deyhdrocholesterol in plasma membranes of epidermal keratinocytes and dermal fibroblasts converted to previtamin D3 by UVB
-15-25 mins whole body exposure produces up to 10,000 IU vit D

281
Q

Can vitamin D be stored?

A

-Yes
-Lipid soluble so stored in subcutis adipocytes

282
Q

Describe the skin as a site of hormone action:

A

-Androgens act on follicles and sebaceous glands
-Thyroid hormones act on keratinocytes, follicles, dermal fibroblasts, sebaceous glands, eccrine glands

283
Q

Describe the skin as a site of hormone synthesis:

A

-Vitamin D3 unique production site
-17beta-hydroxysteroid dehydrogenase in sebocytes and 5alpha reductase in dermal adipocytes convert dehydroepiandrosterone (DHEA) and androstenedione to 5alpha-dihydrotestosterone
-IGF binding to protein-3 (IGFBP-3) synthesised by dermal fibroblasts

284
Q

What rays is the skin a barrier to?

A

Both UV-A and UV-B as they damage the skin

285
Q

What do UV-A and UV-B do?

A

-Burns
-Suppress action of Langerhans cells
-Photo-aging
-DNA damage (skin cancers)

286
Q

What does skin colour depend on?

A

-Melanin
-Carotenoids
-Oxy/deooxyhaemoglobin

287
Q

What is melanin synthesised by?

A

In melanosomes within melanocytes from tyrosine

288
Q

Where is melanin transported?

A

Via dendrites to adjacent keratinocytes

289
Q

What are the two types of melanin?

A

-Pheomelanin (red/yellow)
-Eumelanin (brown/black)

290
Q

What are the deleterious effects of melanin?

A

-Prone to photodegradation – may generate ROS
-Pheomelnin increases release of histamine
-Lots of melanin = less able to utilise UV light to make vitamin D

291
Q

What are the three stages of response to sunlight?

A

-Immediate pigment darkening
-Persistent pigment darkening
-Delayed tanning

292
Q

Describe the immediate pigment darkening in response to sunlight:

A

-Photooxidation of existing melanin
-Redistribution of melanosomes
-Occurs within minutes and lasts hours-days

293
Q

Describe the persistent pigment darkening response to sunlight:

A

-UVA> UVB
-Oxidation of melanin
-Occurs within hours, lasts 3-5 days

294
Q

Describe the delayed tanning response to sunlight:

A

-Increased melanin synthesis
-Occurs 2-3 days after UV exposure, maximal at 10-28 days

295
Q

How do different skin types respond to sunlight?

A
296
Q

Describe the skins function as a barrier to infection:

A

-Properties that render the skin a barrier to water also helps prevent infection
-A range of peptides synthesised by granular layer keratinocytes have antimicrobial properties (cathelicidin-related antimicrobial peptide, b defensins

297
Q

What immune functions does the skin have?

A

-Innate and acquired immune functions
Epidermis:
-Langerhans cells
Dermis:
-Regulatory T cells
-Natural killer cells
-Dendritic cells
-Macrophages
-Mast cells

298
Q

Describe the immune properties of the epidermis:

A

-Keratinocytes secrete cytokines and chemokines that maintain populations of leucocytes in skin
-Langerhans cells are antigen-presenting cells and secrete cytokines

299
Q

What do langerhan cells do in the epidermis?

A

-Migrate to dermis and lymph nodes and activate a T-cell response
-Keratinocytes proliferate and secrete cytokines
-Leucocytes enter skin from blood

300
Q

What three structures give the skin its sensory functions?

A

-Merkle cells – basal epidermis (light touch)
-Encapsulated mechanoreceptors in dermis
-Myelinated and unmyelinated sensory nerve endings in dermis (pain, itch, temperature)

301
Q

What three structures give the skin its sensory functions?

A

-Merkle cells – basal epidermis (light touch)
-Encapsulated mechanoreceptors in dermis
-Myelinated and unmyelinated sensory nerve endings in dermis (pain, itch, temperature)

302
Q

What are the two types of encapsulated mechanoreceptors in the dermis?

A

-Pacinian corpuscles (pressure/vibrations)
-Meissner corpuscles (touch)

303
Q

What 4 things does the skin have to regulate body temperature?

A

-Insulation: (subcutaneous fat)
-Heat loss:
-Cutaneous blood flow
-Eccrine sweating
-Hair

304
Q

Describe the cutaneous blood flow and its role in regulating body temperature:

A

-Deep vascular plexus (lower reticular dermis0
-Superficial vascular plexus (upper reticular dermis
-Loops of blood vessels from superficial plexus extend to reticular dermis

305
Q

What is the equation for heat storage?

A
306
Q

What does evaporation from the skin depend on and what can add or remove heat?

A

-Surface area exposed to environment
-Temp and relative humidity of ambient air
-Convective air currents

-Radiation, conduction and convection can add or remove heat

307
Q

What is the nervous control of the blood flow in dermal vascular plexuses?

A

-Autonomic regulation of blood flow
-Sympathetic alpha-noradrenergic – vasoconstriction
-Sympathetic cholinergic – vasodilation
Both in hairy skin, hairless skin only has adrenergic innervation

308
Q

What is a dual function of sympathetic cholinergic nerves?

A

Sympathetic cholinergic nerves that govern sweating may be the same as those controlling active vasodilation

309
Q

What non-neuronal factor may act on active vasodilation?

A

Nitric oxide may play a role in active vasodilation

310
Q

Describe the sweat release of the skin?

A

-1.6-4 million eccrine sweat glands
-1-3L sweat per hour
-Availability of water is major limiting factor

311
Q

What are goosebumps called?

A

Piloerection

312
Q

Describe piloerection:

A

-Arrector pili muscles innervated by sympathetic alpha1 adrenergic fibres
-Contraction raises cutaneous hairs
-Likely little significant impact on heat conservation

313
Q

What are the functions of subcutaneous fat?

A

-Acts as an insulatpor, shock absorber and energy store
-White adipose connective tissue

314
Q

What are the5 main types of incontinence?

A

-Stress - loss of urine with exertion,sneezing, coughing
-Urgency - leakage accompanied or preceded by urinary urgency
-Moxed - loss associated with urgency and exertion, effort, sneezing or coughing

Not standardised:
-Overflow - leakage associated with retention
-Total - continuous leakage

315
Q

How many nephrons are there in a kidney?

A

-200,000 - 1.8 million

316
Q

What is the blood flow to the kidneys?

A

-1200ml/min
-20-25% cardiac output

317
Q

What is taken from blood to make plasma?

A

-Haematocrit
-Only plasma can cross glomeruli structures

318
Q

What are normal GFR and UO?

A

-GFR = 120ml/min
-Uo = 1.5L/day

319
Q

What are each of these structures?

A
320
Q

Describe the proximal convuluted tubules:

A

-Confined to renal cortex
-Active reabsorption of multiple things - amino acids, glucose, bicarboante, phosphate, salt and water, potassium, chloride, urea
-Metabolically active cells

321
Q

describe renal glycosuria:

A
322
Q

Label reabsorption of glucose in the PCT:

A
323
Q

Describe cystinuria:

A

-AR inherited
-Tubular defect in uptake of amino acid
-Failure of cysteine reabsorption, increased urinary cysteine conc

324
Q

What causes hypophosphataemic rickets?

A

unable to reabsorb potassium

325
Q

What causes proximal renal tubular acidosis?

A

-Na/H antiporter defect
-Failure of bicarbonate reabsorption

326
Q

Describe bicarbonate reabsorption?

A
327
Q

What is fanconi syndrome?

A

-Generalised proximal tubular dysfunction possible due to failure of sodium gradient generation by Na/K ATPase

328
Q

What does the loop of henle do and how?

A

-Generates medullary concentration gradient via countercurrent system
-Active Na reabsorption in thick ascending limb
-Development of a hypertonic interstitium in medullary regions of kidney
-Production of a dilute filtrate entering the distal tubule

329
Q

Describe. theprocess of the ascending limb function:
Drawing a diagram might help

A
330
Q

What does the distal convuluted tubule do?

A

Distal tubule and cortical collecting ducts allow fine tuning of sodium reabsorption, potassium and acid-base balance

331
Q

describe the distal convoluted tubule and how it does its function:

A

-Impermeable to movement of water and sodium
-Uses NCCT co transporter to reabsorb 5% of sodium
-Specific epithelial channel absorbs calcium, paracellular route CA Mg
-Hypokalemia due to increased delivery of sodium to collecting duct

332
Q

Draw the diagram of salt and water transport in the distal convoluted tubule:

A
333
Q

What causes distal renal tubule acidosis (type 1)?

A

na channel defect or H-ATPase so failure to secrete acid

334
Q

What does the collecting duct do?

A

Mediates water reabsorption and maintains acid base homeostasis

335
Q

What are the two cell types in the collecting ducts?

A

-Principal cells - Na and water reabsorption and K excretion
-Intercalated cells (alfa and beta) - secrete H or HCO3

336
Q

What are the main functions of the two cells types of the collecting duct?

A

Principal:
-ENaC - specific Na transporter and main site of Na regulation
-Aldosterone increases the number. ofopen ENaC channels
Intercalated:
-Essential for acid-base homeostasis

Phase 1 (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions