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High-Yield Physiology Notes/Points for USMLE Step 1 & FCPS Part 1
Below are important points & high-yield Physiology notes for USMLE Step 1 and FCPS Part 1 exams.
We have also included a PDF document which contains important points & high-yield Physiology notes for FCPS Part 1 and USMLE Step 1.
RESPIRATION PHYSIOLOGY
Between trachea and alveolar sac, the respiratory tract divides for 23 times. First 16 divisions are conducting zone up to terminal bronchioles. The rest are gas exchange zones
Movement of diaphragm accounts for 75% change in intrathoracic volume during quite inspiration
Most of the work of breathing(65%) is to overcome ELASTIC RECOIL (past MCQ). Other are airway resistance(28%) and viscous resistance (7%)
In the upright position, the ventilation per unit volume is greater at the base of the lung than that of apex… the reason is intrapleural pressure is less negative at the base so alveoli are less expanded. At the apex, the intrapleural pressure is more negative and alveoli are more expanded i.e. the %age of max lung volume is greater. Because of the stiffness of the lung, the increase in lung volume per unit increase in the pressure is smaller when lung is initially more expanded so ventilation is consequently more at base
Exercise is reported to increase the 2,3 DPG in 60 minutes… but n trained athletes this rise may not occur
Four important functions of Hb. 1. Transport of O2. 2. Transport of CO2. 3. Buffer. 4. Transport of NO
Chloride shift is mediated by a protein called BAND 3 one of the major membrane proteins.
Of approximately 49ml of CO2 in dl of the ARTERIAL blood 2.6 ml is dissolved, 2,6 ml is carbamino compound and 43.8 ml is in bicarb form. In tissue 3.7 ml is added. O.4 ml stays in solution, o.8 ml forms carbamino compound and 2.5 ml forms bicarb
Carotid and aortic bodies(GLOMUS) is made of TYPE I and TYPE II cells surrounded by fenestrated sinusoidal capillaries. Type I cells are called glomus cells which resemble chromaffin cells of adrenals and release catecholamines upon exposure to hypoxia and cyanide
Total circulating blood is 8% of total body weight
Active bone marrow forming the blood cells is called red marrow and inactive marrow is called yellow marrow. Inactive marrow is filled with fats.
75% bone marrow belongs to white blood cells producing myeloid series
Neutrophils and monocytes are produced from a single precursor. There are se[arate pools for progenitors of megakaryocytes, lymphocytes, erythrocytes, eosinophils, and basophils
Mast cells, Kupfer cells, dendritic cells, osteoclasts and Langerhans cells also originate from bone marrow
Best source of hematopoietic stem cells is umbilical cord blood
Average half life of neutrophils in circulation is 6 hours
Nutrophils, eosinophils, and basophils are collectively called granulocytes/polymorphonuclear cells
Eosinophils are abundant in GIT and respiratory mucosa
Mast cells are abundant in areas rich in connective tissue eg beneath epithelium
Monocyte leave the circulation and become macrophages in tissues. They do not reenter the circulation.
Pluripotent uncommitted stem cells become committed by the action of IL1, IL6 followed by IL3(I,3,6 commits the stem cells, kind of love guru )
Cytokines are hormone like molecules that act generally in paracrine fashion
IL1 increases slow wave sleep and reduces appetite
Platelets don’t have nuclei.They have half life of 4 days
Splenectomy causes an increase in circulation platelets.
Cytoplasm of platelets contains actin, myosin, glycogen, lysosomes, and two types of granules: a. Dense granules: they have nonprotein substances. They contain serotonin and ADP b. Alpha granules: contain clotting factors, PDGF
Platelet production is controlled by colony stimulating factor and thrombopoietin. Thrombopoietin controls the maturation of megakaryocytes and is produced by kidney and liver.
Osmotic fragility of RBC starts at 0.5% saline. Almost half the RBCs are lysed at 0.40 to 0.42% saline. Complete lysis occurs at 0.35% saline.
2.5 % hb in adults is HbA2
Hb F has the ability to decrease the polymerization of deoxygenated HbS. Hydroxyurea causes HbF production and is used in treatment of HbS
Blood group antigens are called aglutinogens
Blood group antibodies are called agglutinins
Blood group antigens are also present in salivery gland, saliva, kidney, pancrease, liver, lungs, testes, semen, and amniotic fluid
A and B antigens are actually oligosaccharides that differ in their terminal suger. In RBCs they are mostly OLIGOSPHINGOLIPIDS and in other tissues they are glycoprotiens.(past MCQ)
An antigen called H antigen is present in all RBCs in all individuals. In blood group A the A antigen is attached to H antigen, in blood group B the B antigen is attached to H antigen where as in blood group O no antign is attached to H antigen i.e terminal part of blood group O is H antigen(past MCQ). Blood group AB has both antigens at the terminal.
Bilirubin rarely penetrates Blood brain barrier in adults. But in neonates and fetus the BBB is permeable to it an in erythroblastosis feotalis it causes KERNICTERUS
If whole blood is allowed to clot and clot is removed, remaining is called serum. (plasma minus factor 2,5,8,fibrinogen is called serum)(past MCQ)
Serum has high serotonin level due to breakdown of platelets.
Thrombomodulin is produced by all endothelial cells except that of microcicculation of brain
Thrombin is procoagulant in circulation blood. It becomes anticoagulant when it binds to thrombomodulin
Lymph has lower protein content than plasma.
Blood Storage
Storage of different blood products
Whole blood is stored at 4° C for 3 weeks.
Packed cells (RBCs) are stored at 1-6° C for 35 days.
FFP (fresh frozen plasma) and cryoprecipitate can be stored at -40° C for 2 years.
Platelets are stored at 22° C for 5 days
mitral regurgitation =pansystolic murmur
mitral stenosis =mid diastolic murmur
aortic regurgitation =end diastolic murmur
aortic stenosis =ejection Systolic murmur
pulmonary regurgitation =diastolic murmur
pulmonary stenosis =Systolic murmur
throtoxicosis=innocent murmur
decrease hematocrit =continuous murmur
Gastric Motility increased by GASTRIN
Gastric Motility decreased by CCK
Intestinal Motility increased by CCK
Intestinal Motility decreased by SECRETIN
Gastric Emptying increased by Motilin
Gastric Emptying decreased by CCK
Gastric secretions inhibited by SECRETIN
If Newborn to 14 years of age the most common cause is acute lymphoblastic leukemia
If age is between 40 to 60 most likely cause will be AML and CML
If age is more than 60 most likely causes r CLL and CML.
Repeated blood Transfusion…..HAEMOCHROMATOSIS
Multiple Transfusions….HYPOCALCEMIA
Massive Transfusion. ….HYPERKALEMIA, HYPOCALCEMIA, and HYPOTHERMIA
1. Pronephros – degenerate @ week 4
2. Mesenephros – 1st trimester kidney then form male internal genitalia, ureteric bud extends into metenephros to form Collecting Duct, Renal Calyces, Renal Pelvis, Ureter.
3. Metenephros – permanent kidney – forms glomerulus through the distal tubule.
Which kidney is harvested for transplant and why?
1. Left Kidney because it has a longer renal vein
How much of TBW is intracellular vs. extracellular?
1. 1/3 is extracellular
-> 25% is plasma volume
-> 75% is interstitial volume
2. 2/3 is intracellular
What is the 60-40-20 rule?
1. TBW = 60% of Total Body Weight
2. ICF = 40% of total body weight
3. ECF = 20% of total body weight
What is measured to determine plasma volume?
1. Radiolabeled albumin – look at distribution
What is used to measure extracellular fluid volume?
1. Inulin – can distribute to plasma compartment and interstitial volume but not into the cells
How do you calculate the intracellular fluid volume?
1. Total body water – (ECFV via inulin)
What happens to GFR, RPF and the filtration fraction if blood plasma protein concentration increases?
1. RPF does not change
2. GFR decreases
3. Filtration fraction decreases
What happens to RPF, GFR, and the filtration fraction if blood plasma protein concentration decreases?
1. RPF no change
2. GFR increases
3. Filtration fraction increases
What happens if there is constriction of the ureter to RPF, GFR, FF?
1. RPF NC
2. GFR decrease
3. FF decrease
How do you calculate reabsorption and secretion amounts for a given filtered substance?
1. @ 160mg/dL, Na/Glucose cotransporters in the proximal tubule become saturated @ 350mg/dL (plateau of the reabsorption rate).
Why might there be glycosuria and aminoaciduria in pregnancy?
1. Decreased reabsorption of glucose and amino acids at the level of the proximal tubule.
What 3 things increase renin secretion from the JGA?
1. B1 receptor activation on the JGA
2. Decreased Na delivery to the MD in the distal convoluted tubule
3. Decreased BP sensed @ the JGA
Why does decreased Na delivery to MD cause an increase in renin secretion?
1. Decreased Na delivery means more Na is being reabsorbed proximally in response to lower fluid volume, thus need to increase volume (renin secretion)
What are the 5 primary actions of ATII?
1. ATI receptors in vasculature = vasoconstriction
2. Increased Aldosterone secretion
3. Increased Na/H exchanger activity in PCT to increase Na, HCO3, and H20 reabsorption
4. Increased ADH from posterior pituitary (supraoptic nucleus via neurophysins)
5. Increased thirst (hypothalamus)
Where is Angiotensin Converting Enzyme located?
1. Lungs and Kidney –> Remember it is important for the degredation of bradykinin, inhibition can potentially lead to angioedema.
What does ADH primarily respond to?What does ADH primarily respond to?
1. Decreases in osmolarity (remember this is sensed by the osmoregulator fenestrated areas in the brain)
– At very low volume, ADH will be secreted
What does Aldosterone mostly respond to?
1. Decreases in blood volume
How does ANP regulate volume?
1. Leads to vasodilation via release of cGMP and then NO
2. Increases the GFR and increases Na excretion without increases in proximal tubule Na reabsorption. to net volume loss and Na loss
–> This is why in hyperaldosteronism you will have normal fluid volume with hyponatremia, hypernatremia, and increased bicarbonate.
What substances/changes will shift potassium out of the cell?
DO Insulin LAbs:
Digitalis
HyperOsmolarity
Insulin deficiency
Lysis of Cells
Acidosis
Beta Antagonists (anti catabolic)
What substances/changes shift potassium into cells? (4)
What are the causes of normal anion gap metabolic acidosis?
HARD ASS
Hyperalimentation
Addison’s Disease
Renal Tubular Acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline Infusion
1. What is Type 1 renal tubular acidosis?
2. What kidney stones is a person with type 1 RTA at risk for developing?
1. Defect in collecting tubule’s ability to excrete H+ ions -> Resulting in hypokalemia, acidosis,
2. Increased risk of calcium phosphate kidney stones because increased pH or urine (>5.5)
1. What is Type 2 renal tubular acidosis?
2. What is the effect on potassium levels and what disease state is it associated with?
3. What is urine pH?
1. Defect in PCT ability to reabsorb HCO3- resulting in hypokalemia (at the distal collecting tubule/duct)
2. Fanconi’s Syndrome
3. Urine pH is <5.5 (Collecting duct and distal tubule can still secrete H+)
1. What is Type 3 renal tubular acidosis?
2. What happens to urine pH in type 3 RTA?
1. Hypoaldostronism – decreased collecting tubule response to aldosterone resulting in hyperkalemia
2. Urine pH will decrease because hyperkalemia messes up ammoniagenesis and thus NH3 buffering capacity
Nerve Cell Physiology
Describe the basic components of a nerve cell
Dendrites – receive and integrate input
Soma/Cell Body – location of nucleus
Axon – carrier of action potential to presynaptic terminal
Axon hillock – demyelinated, where action potentials are generated
Myelin sheath – insulates axon and aids action potential conduction
Nodes of Ranvier – boosting stations for action potentials between myelin sheaths
Presynaptic terminal – end of axon that releases neurotransmitters to pass a signal to another neuron
Describe the nature of ionic permeability of the cell membrane
The lipid bilayer is impermeable to ions. Ion channels allow ions to cross the membrane. Ion pumps use energy to maintain the concentration gradients across the membrane.
Explain how the resting membrane potential is generated
Two forces work on ions: passive diffusion (moving down a concentration gradient) and electrostatic (repelling like forces). The electrostatic force generated by the separation of charged ions across the membrane prevents the complete diffusion of ions down their concentration gradients via ion channels. The net flow of ions across a cell membrane will be zero when the electrostatic and diffusion forces reach an equilibrium. The resting potential of a cell membrane is determined by the concentrations of ions present and their relative permeabilities across the membrane.
Explain how the action potential is generated
Applied current or excitatory input — voltage-gated Na+ channels open and Na+ rushes into cell — cell membrane is depolarized — Na+ channels begin to close as slower voltage-gated K+ channels open — cell membrane repolarizes and “undershoots” to cause an afterhyperpolarization — K+ channels close and membrane returns to resting potential
Explain the cause of the “refractory period” following action potential generation and discuss its functional significance
The Na+ channels have an inactive state following activation and cannot generate another action potential. Also, the opening of K+ channels hyperpolarizes the cell so that the membrane is unable to generate action potentials of equal strength. The refractory period limits how soon one action potential can be followed by another.
Explain how membrane potentials spread passively
In the absence of an action potential and voltage-gated Na+ channels, an injected current will travel passively down the axon. The magnitude of the current pulse decays exponentially, like a “leaky hose.”
Explain how action potentials propagate actively
Depolarization opens more Na+ channels farther down the axon, which causes further depolarization in a positive feedback cycle.
Explain why myelination allows for faster propagation of action potentials and how demyelination affects action potential conduction
Myelination increases the membrane resistance, which prevents leakage of ions, makes the length constant of the axon longer, and current can spread farther before decay. Myelination decreases the membrane channels’ capacitance (the resistance to ion flow) , which decreases the time constant, and the membrane can depolarize faster.
Demyelination increases the membrane capacitance, requiring more local current to depolarize for an action potential. The membrane resistance is lower, meaning a shorter length constant and limited spread of the local current. Action potentials are slowed or blocked in diseases of demyelination.
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