Human phys IV Flashcards
1
Q
4 basic processes of the digestive system
A
1 motility (propulsion and mixing)
2 Digestive
3 secretion (exo and endo (into circulatory sys))
4 absorption
2
Q
digestive tract from inside out ()
A
lumen -> lamina propria -> Muscularis mucosa -> submucosa -> muscularis externa
3
Q
what makes up the mucosa
A
endothelial cells, lamina propria, muscularis mucosa
4
Q
What is splanchnic circulation?
A
It involves the hepatic portal system
it forces blood to go through the liver after picking up nutrients along the digestive tract
5
Q
what are hypatocytes?
A
cells that line the sinusoids of the liver.
They produce bile that gets stored in the gallbladder until needed for digestion
6
Q
What’s special about sinusoids?
A
They have blood mixed from two sources in em
from the Hepatic artery and hepatic portal vein
7
Q
Why deliver absorbed products from the liver?
A
1 metabolic processing
2 storage
3 detox
4 removal of bacteria
5 conservation of bile salts
8
Q
What pathways regulate GI activity?
A
endocrine - hormone in bloodstream
paracrine - hormone into interstitial fluid
autocrine - self activate in absence of stimulus
neuronal - nerves
9
Q
What is the enteric nervous system?
A
part of the autonomic nervous system and is intrinsic –
composed of the submucosal and myenteric plexus
10
Q
how does the CNS influence the enteric nervous system
A
parasympathetic: increases digestion and signals via the vagal nerve and spinal cord
sympathetic: lowers digestive activity
11
Q
GI smooth muscles are…
and
how do they excite?
A
single-unit and constrict as a unit (functional syncytium)
self-excites with slow wave potentials or a basic electrical rhythm (BER)
12
Q
Basic electrical rhythm
A
constant frequency but amplitude varies
at threshold sends an AP for Ca++ to be released -> leading to constriction
13
Q
How does amplitude change within GI smooth muscles?
A
pacemaker cells (interstitial cells of Cajal) within the myenteric plexus
14
Q
3 types of GI motility
A
peristalsis = moving food along
rhythmic segmentation = mixing by constricting along both ends of material
tonic contraction = divide bolus
15
Q
what do muscle do along peristalsis? (list)
A
distension of gut wall leads to stretch
sensory neurons relay signal to the myenteric plexus
interneurons transmit signal in both directions
smooth muscle contracts behind bolus and relaxes in front.
16
Q
What is receptive relaxation
A
in the proximal stomach in response to distension
this activates the vagal nerve
17
Q
pyloric sphincter 😊
A
end of the stomach
if food is too large to fit through it is STOPPED and RETROPULSED back
18
Q
How does the CNS affect gastric motility?
A
the vagal efferent nerve sends a signal to the enteric nervous system
this sends a signal to the stomach wall G-cells
which produce gastrin and increase gastric motility
19
Q
How to decrease gastric motility?
A
duodenum products cause reactions:
HCl -> S cells -> secretin
Fat and a.a.s -> I cells -> CCK
receptors trigger CNS and enteric nervous systems
all of these decrease motility
20
Q
interdigestive period
A
time b/w meals
21
Q
MMC?
A
migrating motor process -happens every 90 minutes. They are initiated by motilin (via M-cells)
suppressed by food intake (Gastrin and Ach which is a parasympathetic NTS)
22
Q
How are salivary glands dually innervated?
A
sympa: more mucousy
parasympa: rich in enzymes
23
Q
saliva composition
A
1) mucus (trap water, helps lubricate)
2) amylase (breaks down starch) (pH 7-7.4)
3) Bicarbonate (chemical buffer) (makes pH 7-7.4)
4) antimicrobial agents
24
Q
What are a stomach’s infoldings
A
gastric pits, at their base are gastric glands
25
names for the sections of the stomach and what's in em
Fundus - very top
Body -> Oxyntic mucosa
antrum -> Pyloric gland area
26
Oxyntic Mucosa components
* Mucosa – mucus
* Chief Cells – pepsinogen
* Parietal Cells – HCl and intrinsic factor
* Enterochromafin Like Cells (ECL)
– histamine
27
What does pepsinogen do?
Histamine?
when activated as pepsin it digests proteins.
acid production, gastrin activity, G-cell activity
28
Pyloric gland
* G-cells - gastrin, blood flow, parietal cell activity
* D-cells - somatostatin
29
What does Gastrin do>? Somatostatin>?
Gastrin = stimulates G-cells which make pepsin
Somatostatin = master negative regulator
30
What is the function of HCl in the stomach>>
solubilization, killing microbes, activation of pepsinogen.
body makes 2L HCl a day
31
HCl production
carbonic anhydrase converts CO2 into HCO3. Parietal cells excrete H+ and Cl- into the stomach
32
Control of gastric secretion
1) cephalic phase
2) Gastric phase
3) intestinal phase
33
cephalic phase pathway
Gastric phase pathway
sensory info -> parasympathetic nervous system -> Vagal nerve -> AcH and G-cell stimulation -> HCl and pepsinogen production
(Gastric is the same except for stimulation is via stretch receptor in stomach)
34
Intestinal phase
all types of receptors-> lowering of gastric secretion and motility, I and S cells stimulated
35
what are the endo and exocrine tissues of the pancreas>?
endocrine - islets of Langerhans (insulin)
exocrine - secretory cells - acinar cells
36
purpose of pancreatic enzymes and aqueous alkaline solution
the enzymes are released as inactive zymogens
the solution is NaHCO3
37
all of the proteolytic enzymes (5)
trypsinogen (regulated by enteropeptidase)
chymotrypsinogen
procarboxy peptidase
pancreatic amylase
pancretic lipase.
38
pancreatic amylase and
pancreatic lipase functions
digestion of carbohydrates and digestion of fat
39
What regulates pancreatic stimulation?
predominant stimuli of products entering the duodenum
40
Potentiation
antagonism
stronger response when together
like secretin and CCK working together to cause release of pancreatic enzymes
when one hormone reduces the effectiveness of another
41
What are bile salts and what causes their release?
driven by an increase in CCK
synthesized by the liver and are stored in the gallbladder
help emulsify and absorb fats
42
More bile fatcs
released into the duodenum via the sphincter of Oddi
95% gets reabsorbed and small intestine mostly does this
43
Parts of the endocrine system
central glands - pituitary glands - hypothalamus - peripheral (reproduction, thyroid, parathyroid, adrenal)
44
2 main types of hormones
hydrophilic - fast
hydrophobic - slow and require transporter proteins
45
tropic vs trophic hormones
hormones that cause the release of other hormones vs hormones that maintain growth and development of a tissue
46
types of responsive control
down regulation; internalization of receptors for a hormone
permissiveness; one hormone must be present to permit full response
synergism; hormonal actions stack
47
endocrine dysfunction definition
inappropriate amounts of secretion or response
48
pituitary gland (hypophysis)
connected to the hypothalamus via the pituitary stalk
consists of posterior and anterior pituitary
(nervous tissue and glandular epithelial tissue)
49
posterior pituitary
neurosecretory axons star in hypothalamus where peptide hormones are made.
these hormones are stored in the pituitary
VASOPRESSIN and OXYTOCIN
50
Vasopressin
binds to nephrons in kidneys and well as arterioles
increase H2O permeability in distal tube
cause vasoconstriction
51
Oxytocin
Binds to cells in uterus and mammary glands
causes contractions and stimulated milk ejection during breastfeeding
52
Anterior pituitary
neurosecretory axons start in the hypothalamus and STOP at hypothalamic capillaries to release hormones
these flow thru the hypothalamic-hyposeal portal
hypophysiotropic hormones:
inhibiting and releasing
53
releasing vs inhibiting hypophysiotropic hormones
depend on glandular cell hormone release
54
How are the hypothalamus and the anterior pituitary inhibited
via negative feedback
55
hypophysiotropic hormones
Thyrotropin
Corticotropin
Gonadotropin
Growth Hormone
Somatostatin
prolactin releasing and inhibiting peptides
56
Targets of ea of these
Thyrotropin
Corticotropin
Gonadotropin
Thyrotrope
corticotrope
gonadotrope
57
Targets of ea of these
Growth Hormone
Somatostatin
prolactin
somatotrope
somatotrope
lactotrope
58
Thyrotrope pathway
-> TSH -> Thyroid gland -> increased^ metabolic rate
59
Corticotrope pathway
-> ACTH -> adrenal cortex -> cortisol -> Stress response and metabolic response
60
Lactatrope pathway
-> prolactin (H2) -> Mammary glands -> breast growth and milk secretion
61
Somatotrope pathway
-> Growth hormone
-> adipose tissue, muscle, liver ->
metabolic actions
-> IGF-I -> bone and soft tissue -> growth
62
Gonadotrope pathway
-> LH -> ovaries -> Sex hormone secretion and gamete production
-> FSH -> testes -> Sex hormone secretion and gamete production
(present in both sexes)
63
physiological roles of thyroid hormones
1) determinant of growth
2) regulator of overall energy expenditure (basal metabolic rate)
3) Optimizes sensitivity of tissues to other hormones
64
Example of permissiveness
thyroid controls beta adrenergic receptors in the heart
65
components of follicles in the thyroid
1) follicular cells
2) colloid
66
What do follicles make?
a precursor protein called thyroglobulin
is contains tyrosines
67
What is stored in the colloid?
iodinated thyroglobulin
68
How are thyroid hormones excreted?
When TSH stimulates thyroglobulin
(? im not too sure?)
69
Main Effects of thyroid hormone
^BMR
more permissiveness to NE and EPI
70
T3 and T4 pathway from signal in brain to release
Hypothalamus -> thyrotropin-releasing hormone -> anterior pituitary -> thyroid stimulating hormone -> thyroid gland -> thyroid hormone
71
TPO
activates iodide and attaches them to thyroglobulin (Tg)
72
What leads MITs and DITs to become T3 or T4?
a conjugation reaction
73
What gets T3 and T4 out of the thyroid?
TSH induces movement, and T3 and T4 and hydrophobic so they need to bind with thyroxine binding globulin
74
Hypothyroidism and its types
primary: failure of thyroid gland
secondary: deficiency of TRH/TSH
Dietary: inadequate supply of iodine
75
Hypothyroidism causes...
cretinism:
dwarfism
and impaired cognitive function and reduce nerve + muscle reflexes
76
Cretinism
development problems with central nervous system and body growth
impaired cognitive function and delayed motor development
Short stature and protuberant abdomen
77
dwarfism
limited long bone growth (shorter)
impaired cognitive function
78
Hyperthyroidism and its types
disease symptoms
excessive TRH and TSH
Causes grave's disease
- Disease that produces TSI
Symptoms; exophthalmos
opposite of other symptoms and bulging eyes
79
How does a goiter form?
Hypo: no T3/4 from diet or gland failure
Hyper: excess TSH
80
Cortisol axis
stress + diurnal rhythm ->
Hypo ->
CRH ->
Anterior pituitary ->
ACTH ->
Adrenal cortex ->
cortisol (which inhibits hypothalamus and anterior pituitary)
^increased blood glucose, a.as, and fatty acids
81
What is the adrenal gland composed of? What do they secrete?
adrenal cortex -> outer layer producing steroids (cortisol)
adrenal medulla -> inner layer producing catecholamines (EPI)
82
layers of the adrenal gland
top to bottom
zona... glomerulosa (makes aldosterone),
fasciculata (makes cortisol),
reticularis (makes DHEA),
medulla
83
Steroid hormone pathways
cholesterol
-> pregnenolone (stimulated by 17alpha hydroxylase)-> DHEA
-> pregnenolone -> aldosterone
84
Example of a mineralocorticoid and what it does (all about it)
ADOSTERONE
increases Na reabsorption and K+ secretion [very important dude] -> maintains blood pressure too
regulated thru RAAS
85
Example of a Sex hormone and what it does (all about it)
| (main one of the ADRENAL gland)
DHEA
similar to testosterone and no affect in males. Influences growth of hair, sex drive, and pubertal growth spurt
86
What do glucocorticoids do? What's the main one>?
Cortisol
It increases blood glucose via gluconeogenesis
dampens immune response, helps you adapt to stress, changes permissiveness of other hormones
87
Cortisol pathway
Hypo -> CRH -> anterior pituitary -> ACTH -> adrenal cortex -> cortisol
88
Diurnal regulation
idk dood
affects CRH, then ACTCH, then cortisol in light and dark waves.
89
Cushing's syndrome
too much cortisol!
adrenal cortex too stimulated: TOO MUCH CRH/ACTH
hyperglycemia, Glucosuria, abnormal fat distributions, muscle weakness, thin skin, osteoporosis
90
Adrenocortical Deficiency information
(primary)
primary - Addison's disease
all three layers of adrenal gland underproduce and autoimmune disease leads to destruction of adrenal cortex
91
Adrenocortical Deficiency information
(Secondary)
* Occurs due to pituitary-hypothalamic problems (decreased CRH/ACTH)
* Only cortisol is deficient!
92
ADRENAL ANDROGREN HYPERSECRETION
too much ACTH and DHEA too little cortisol
causes hirsutism in females (masculinizing effects)
93
Main features of adrenal medulla
parts of sympathetic nervous system
made of modified postganglionic neurons called chromaffin which release Epinephrine
roles in stress responses, arterial blood pressure and controlling fuel metabolism
94
Stress is regulated by the hypothalamus. What are all the physical reactions to it?
* Increased sympathetic activation and
epinephrine release
* Elevate blood glucose and fatty acids
* Inhibit insulin secretion
* RAAS through sympathetic activation of
kidney
* Activation of the CRH-ACTH-cortisol axis
95
== free space ==
BD
96
absorptive vs postabsorptive states
fed vs not fed (4 hours after eatin)
97
Primary brain fuel source? what doesn't the brain store?
glucose, glycogen
the brain takes precedence over other tissues and can even resort to ketones for energy
98
What is glucogenesis>?
glycogenesis>?
glycogenolysis>?
converting a.a.s to glucose
glucose->glycogen
glucose<-glycogen
99
What hormone lowers blood glucose levels?
insulin
100
ENDOCRINE PANCREAS
Physiological Roles:
* Regulate whole body macronutrient
metabolism
* Coordinate whole body metabolism after
ingestion and while fasting
Islets of Langerhans too
101
types of cells in the Islets of Langerhans
* Alpha cells – glucagon producing cells
* Beta cells – insulin producing cells
* Delta (D) cells – somatostatin
* F cells – pancreatic polypeptide
* Epsilon Cells - Ghrelin
102
How does Insulin decrease blood glucose levels>
1) facilitates transport into cells
2) stimulates gluconeogenesis
3) Inhibits glycogenolysis
4) stimulates glycogenesis
103
What does only insulin do that other hormones don't?
Insulin is the ONLY hormone capable of lowering blood glucose
104
excitation-secretion coupling
1) Glucose goes into cell via GLUT-2
2) converted into glucose-6 phosphate
3) Oxidized and produces ATP
4) ATP-sensitive K+ channel closes
5) Depolarization
6) voltage-gated Ca2+ channel opens
7) vesicular release
105
GLUT-4
responsible for most glucose uptake in body cells* Resting skeletal muscles and adipose
tissue
* These account for bulk of glucose
uptake during absorptive state
* Normally not present in cells,
insulin inserts it into the plasma
membrane
106
Insulin Independent Transporters:
in brain, liver, kidney, neurons, and skeletal muscles DURING excercise
107
Glucagon
released by alpha cells in postabsorptive state
does the opposite of insulin
108
DIABETES MELLITUS types
Type one (insulin dependent)
Type two diabetes (insulin independent)
109
Type one diabetes
Caused by beta cell destruction or autoimmune disorder (not enough insulin production)
* Elevated blood glucose
* Polydypsia: frequent drinking, osmotic stress
* Polyuria: frequent urination
110
Type two diabetes (90% of cases)
not enough insulin or tissue resistance to insulin.
a post-receptor defect that requires more insulin to produce an affect.
111
YAY!
YAY!
112
What are the most abundant inorganic elements in peopel
calcium and phosphate
113
Physiological roles of calcium and phosphate
neuromuscular excitability
excitation-contraction in cardiac + smooth muscles
stimulus secretion coupling
excitation secretion coupling
formations+maintenance of bones+teeth
114
phosphate and calcium levels are monitored by...
tissues- kidney (amnt secreted) intestine (absorption)
hormones- parathyroid hormone, primary regulator is vitamin D , calcitonin (emergency)
115
PTH
parathyroid hormone:
released from parathyroid in response to low calcium
regulates osteo-clast and blast to release calcium into bloodstream
lowers plasma phosphate
116
chronic hypocalcemia
too little calcium in blood because bones are growing faster than disassembling
117
Pathway for vitamin D to lower calcium levels in blood
precursor in skin -> sunlight -> vitamin D (also gotten from digestion system) -> liver enzymes -> activated vitamin D -> kidney enzymes -> intestine -> ^calcium reabsorption
118
what needs to activate vitamin D
kidney and liver
119
Rickets
due to calcium deficiency;
hypocalcemia and bone abnormalities
-kidney stones, thinning of bones, bowing of legs, growth retardation, poor mineralization
120
adult calcium deficiency
osteomalcia, malformed bones, lower phosphate levels due to renal phosphate wasting
121
All parts of the reproductive system
goNADS
reproductive tracts
accessory sex glands
122
names of the production of sperm and eggs
spermato and oogenisis
123
sparm pathway
testes -> epididymis -> Ductus (vas) deferens -> ejaculatory duct -> urethra
124
Who's wolf grows up and whose gets eaten by the body (IMPORTANT)
girlies eat theirs because they metal as hell
125
egg pathway
ovary -> fallopian tubes -> uterus -> thru cervix
126
whats special about gametogenisis
its produces genetically distinct sperm and ova
127
What is the first decisive point in becoming a sex?
ySRY gene
128
ySRY makes...
TDF or testes determining factor
129
ducts after differentiation of sex
mullerian ducts degenerate in males, wolffian in females
130
