Revision Flashcards
What do intercalated and principle cells do in the DCT?
Intercalated:
- H+ secretion
- K+ resorption
Principle cells:
- Na resorption
- K+ secretion
Acid- Base Balance: In the Kidneys how is HCO3 reabsorpbed and where?
PCT:
- Carbonic anhydrase
- Na reabsoprbed & H+ excretion
DCT:
- Intercalated cell: (both on tubular membrane)
- H+ ATPase
- K/H ATPase (H out, K in)

Acid Base Balance: How is H+ secreted in the Kidneys
Late DCT:
Intercalated cell A:
- H+ ATPase
- K/H ATPase
However this is not sufficient on its own so you need: URINARY BUFFERS- as both below processes occur HCO3- is made and being added to blood
Phospahte:
(I think anywhere this can happen)
- Na/ H exchanger (Na in and H out)
- NaHPO4- combines with H+
Ammonia:
- In PCT Glutamine synthesied to form NH4+
- In CCT: NH3 secreted. H+ATPase secretes H+ which combine to make NH4+

a) Where does Gluconeogenesis occur?
b) Where do glycogenolysis occur?
a) Liver & Kidneys
b) Liver & Skeletal muscle
What transports Iodide into the follicular cell?
Na/ I symporter
What converts iodide into iodine?
Thryoid peroxidase
What take iodine from the follicular cells –> Colloid?
Pendrin
Where is thyroglobulin synthesised?
In the follicular cell
Why type of hormone is the thyroid hormone?
Therefore how does it travel in blood?
Steroid hormone
70% Thyroid Binding Globulin
30% Albumin
What does thyroid binding globulin have a higher affinity for?
T4
How does T3 have an action on target cells?
T3/ T4 enters cell via: Diffuse/ Transported MCT 8(10)
T4 –> T3 via deiodinases
T3 binds to intracellular receptors (alpha or beta)
Interacts and binds w/ DNA and changes protein synthesis
Describe the types of deiodinases- where are they found?
Type 1: T4 –> T3 Activates inner and outter ring. Found on most cells- liver, kidney, brain, thryoid
Type 2: T4 –> T3 Activates outter ring. Intracellular raise- CNS, brown fat, placenta, MSK, SK/ Cardiac muscle
Type 3: T3–> T2 or T4 –> rT3. Remove T2- placenta/ CNS
What are the physiological actions of T3?
- Metabolism (increase BMR)
- Maturation & Differentiation- Bone, lungs & Brain
- Neurological Function- Synapse formation, myelinogenesis, Neuronal outgrowth
-
Growth: CNS/ Skeletal development
- Regulated by GH but T3/T4 needed
- By 12 week of gestation gland makes/ secretes t3/t4 so need suficient iodine from mother
Beyond insulin and glucagon give some hormonal examples of glucose control
- Adrenaline- increase glucose production and lipolysis
- Cortisol- increase glucose production and lipolysis
- Growth Hormone- increase glucose production and lipolysis
- FFA- increase glucose production
- Incretins eg: GLP-1
Describe how insulin is secreted
1) Extracellular glucose is transported into B cells via GLUT 2
2) Metabolised to ATP which increases the ATP: ADP ratio in cell
3) Cause closure of ATP dependant K+ channels
4) –> Depolarisation of cell membrane
5) –> Influx of caclium via voltage gated calcium channels
6) –> Exocytosis of insulin from stored vesicles
Talk about the stages of biphasic insulin secretion:
Stage I: Rapid onset and lasts 10 mins
Release of pre-docked & primed vesicles
Stage II: Prolonged plateau. As long as hyperglycaemia exists
Transport –> Dock –> Prime –> Fusion
Talk about how insulin promotes glucose –> Cell
Anabolic (Promote Glycogen synthase, Lipogenesis, Protein synthesis & Mitogenesis. Prevent Protein and lipid breakdown)
Bind to GLUT 4 receptor on cell membrane
GLUT 4 stored in IC vesicles. Insulin promotes vesicular fusion & transportation and insertion into the wall. Causing glucose –> cell
Fed State: Entero-Insular Axis:
What are the two hormones produced?
Where are the produced from?
What are they produced in response to?
What are they degraded by?
Gastrointestinal Insulinotropic Peptides: Gastric Inhibitory Peptide, Glucagon Like Peptide
Produced by L cells of SI
Produced in response to oral glucose load to augment insulin secretions
Degraded by: Dipeptidyl-peptidase 4
What causes DMT1?
What are the 4 Cardinal symptoms?
What is DKA caused by? Symptoms? Causes?
AI disease, selective destruction on pancreatic B cells –> complete insulin deficiency
Symptoms: Weight loss (unopposed proteolysis & lipolysis), Polydyspia, Polyuria, Hyperglycaemia
DKA: Production of KB (from b oxidation of FA) as alternative energy source. Symptoms: High RR, Abdo pain. Causes: Preceed illness/ missed insulin dose
What are the complications (bar hyperglycaemia) of DM. Split into Macrovascular and Microvascular
Macrovascular:
- Nephropathy
- Retinopathy
- Neuropathy
Microvascular:
- IHD
- PVD
- Cerebrovascular disease
What type of hormone is insulin?
Peptide hormone
GLUT 1:
Affinity
Specificity
Tissue Distribution
Notes:
Affinity: 1.5mM
Specificity: Glucose, Galactose, Mannose
Tissue Distribution: Ubiqutos, RBC, Brain
Notes: low affinity increase basal uptake
GLUT 2:
Affinity
Specificity
Tissue Distribution
Notes:
Affinity: 15mM
Specificity: Glucose, Fructose
Tissue Distribution: Pancreatic B cells, Liver
Notes: high affinity therfore low basal uptake
GLUT 3:
Affinity
Specificity
Tissue Distribution
Notes:
Affinity: 1.8mM
Specificity: Glucose
Tissue Distribution: Brain, intestine, placenta
Notes:











