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M1 Block 5 > Week 3 > Flashcards

Week 3 Flashcards

1
Q

What is the pediatric compression: breath rate for CPR?

A

15:2

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2
Q

What is the maximal time for pausing compression for breath administration?

A

10 seconds, each breath should be 3 seconds

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3
Q

Why is a common cause of cardiac arrest in adults? What BLS activity will restore function, normally?

A
  • Heart problem i.e. V fib
  • Resuscitation by AED
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4
Q

What are 2 reasons to administer compressions on someone with a pulse?

A
  • HR (less than 60) too low & not perfusing
  • Choking
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5
Q

What is the age range to use pediatric AED pads?

A

8 yr of age or less use pediatric

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6
Q

Where are the 2 AED pads placed on an adult?

A
  • L: below the nipple line
  • R: chest
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7
Q

When is the only appropriate time to stop chest compressions for more than 10 seconds in BLS?

A

When the AED is analyzing rhythm

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8
Q

T/F: If applying AED to person in water, snow, or puddle you must move them before administering a shock

A

False, only need to move person if they are in shallow water to administer shock

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9
Q

In BLS, when using a bag mask, how much should the bag be compressed to administer respiration?

A

Only need to administer about 1/2 the bag
Watch for chest rise!

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10
Q

When can you administer breaths and compressions together in CPR?

A

When there is an advanced airway in place can administer chest compressions and respirations

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11
Q

During CPR, how often to check person’s pulse?

A

~ every 2 minutes

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12
Q

What are parameters for determining “child” age in BLS/CPR administration?

A

1 yoa-puberty (presence of body hair)

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13
Q

What is the compression:breath rate for 2 person CPR team administering on a child?

A

15 compression: 2 breath

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14
Q

Infant CPR: When to use two handed compression technique?

A

When there is a two person team working on CPR for infant with 15:2 compression ratio

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15
Q

What is the downstream signaling of Gαq

A

2 Pathways:
1. IPC 3 to release intracellular Ca+2
2. DAG to PCK to phosphorylate TF

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16
Q

What is the downstream signaling of Gαs?

A

Adenyl Cyclase > cAMP > PKA/CREB > induce phosphorylation of TF or Induce transcription, respectively

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17
Q

What is the downstream signaling of G αi?

A

Inhibitory of G α s which normally induces Adenyl cyclase > cAMP > PKA/CREB > phosphorylate TF or induce transcription, respectively

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18
Q

A hormone is a chemical substance classified as:

A

Hormones can be classified as:
1. Steroids
2. Peptides
3. Amines

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19
Q

Where in the body has the highest amount of hormone release?

A
  • Highest hormone release from the Hypothalamus
  • Hormones that are released from the AP are in low concentrations
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20
Q

Compare the relationship between the anterior pituitary and hypothalamus vs. posterior pituitary and hypothalamus

A
  • AP-H: endocrine and neural since the AP makes and releases hormones based on information from hypothalamus
  • PP-H: Neural only since the posterior pituitary does not make any hormones
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21
Q

What is the hypothalamic-hypophysial system?

A

The relationship b/t the hypothalamus and pituitary gland
- Has the hypothalamic-hypophysial portal blood vessels that provide blood supply majorly to the AP and less to the PP

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22
Q

What does TRH stand for and where does it come from?

A

Thyrotropin-releasing hormone
Comes from hypothalamus

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23
Q

What does GnRH stand for and where does it come from?

A

Gonadotropin-releasing hormone
Comes from hypothalamus

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24
Q

What does GHRH stand for and where does it come from?

A

Growth hormone-releasing hormone
Comes from hypothalamus

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25
Q

What is GIRH? Where does it come from?

A
  • GIRH is AKA somatostatin
  • Comes from hypothalamus
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26
Q

What is PIH and where does it come from?

A
  • PIH is prolactin inhibiting hormone
  • Comes from hypothalamus
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27
Q

What are 2 hormones that exhibit positive feedback mechanisms?

A
  • Oxytocin
  • Estrogen/Estradiol
  • Positive feedback is very rare
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28
Q

Estrogen exhibits positive feedback, by what route?

A
  • Short feedback loop acting on FSH/LH in the Ant. Pituitary
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29
Q

What does the posterior pituitary release?

A
  • Oxytocin
  • ADH/Vassopressin
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30
Q

Oxytocin exhibits positive feedback, by what route?

A
  • Short feedback loop acting on the posterior pituitary to release more oxytocin
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31
Q

What is another name for Vassopressin?

A

Antidiuretic hormone

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32
Q

By what mechanisms does Vasopressin act?

A
  1. Induces placement of aquaporins into principle cells of collecting duct to induce reuptake of water
  2. Vascular smooth muscle contraction to increase BP
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33
Q

What do thyrotropes release? Where are they?

A

Thyrotropes are in the AP
Release TSH from the AP

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34
Q

What are gonadotrophs? Where are they?

A

Gonadotropes are in the AP
They induce release of FSH/LH from AP

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35
Q

What are corticotropes and where are they?

A

Corticotropes are in the AP
Induce release of ACTH from AP

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36
Q

What are lactotrophs? Where are they?

A
  • Lactotrophs are in the AP
  • Induce release of prolactin
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37
Q

What does ACTH stand for?

A

Adrenocorticotropic Hormone

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38
Q

TSH, FSH, and LH are all structurally related. What does this mean and how can it be applied to patient therapy?

A
  • They all have α & β subunits
  • Only the β subunits is unique to each hormone
  • This means replacement therapies can mimic all three hormones
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39
Q

Most hormones released from AP are peptides. What is the exception?

A
  • Cortisol and sex hormones are steroid hormones
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40
Q

What does FSH do specifically?

A

F: Stimulates development of ovarian follicles
M: Regulates spermatogenesis in testis

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41
Q

What does LH do specifically Males?

A

M: Production of testosterone by testis

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42
Q

What does LH do specifically Females?

A
  1. Inducing ovulation and formation of corpus luteum in ovary.
  2. Production of estrogen & progesterone in ovary
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43
Q

What is the significance of Pro-opiomelanocortin?

A
  • The precursor of ACTH hormones
  • Also precursor of:
    1. γ& β-lipotropin
    2. β-endorphin
    3. Melanocyte-stimulating hormone
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44
Q

What hormone induces darker pigmentation of the Linea alba in pregnancy?

A

Melanocyte-stimulating hormone which is from POMC

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45
Q

Name the hormones from the anterior pituitary that are derived from Pro-opiomelanocortin

A
  1. Melanocyte-stimulating hormone
  2. . β-endorphin
  3. γ-lipotropin
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46
Q

What embryological tissue is the posterior pituitary derived from?

A

Neuroectoderm

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47
Q

What embryological tissue is the anterior pituitary derived from?

A

Oral ectoderm

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48
Q

What is the difference between actions of prolactin & oxytocin related to breastfeeding?

A
  • Prolactin: Milk production & secretion
  • Oxytocin: Milk letdown in response to suckling
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49
Q

What receptors does ADH act on?

A
  • V1: Smooth muscle BP regulation
  • V2: Serum osmolarity
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50
Q

What is the primary function of Vasopressin?

A

Acting on V2 receptors in response to increased serum osmolarity to induce water reuptake

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51
Q

AHD level is __________________ in central diabetes insipidus.
ADH level is __________________ in nephrogenic diabetes inspidus.

A

ADH level is low in central diabetes insipidus
ADH is normal (even increased) in nephrogenic diabetes insipidus

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52
Q

What is the treatment for Central Diabetes Insipidus? What else does this treatment do?

A
  • Desmopressin used for C DI
  • Can also treat nocturnal enuresis
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53
Q

What are inhibitory factors of ADH secretion?

A
  • Decreased serum osmolarity
  • Ethanol
  • α-adrenergic agonists
  • ANP
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54
Q

What is the cause of Nephrogenic Diabetes Insipidus?

A
  • V2, G α s , adenyl cyclase mechanism defects
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55
Q

What is the treatment for Nephrogenic diabetes?

A

Thiazides cause blood volume contraction which lower GFR so less water is filtered & thus less water can be excreted

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56
Q

What is the blood osmolarity and what is the urine osmolarity in SIADH?

A
  • Blood is dilute
  • Urine is concentrated
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57
Q

What is the treatment for SIADH?

A
  • Demeclocycline
  • Water restriction
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58
Q

What are causes of SIADH?

A
  • ” HEELD - up water”
  • Head trauma
  • Ectopic ADH due to small cell lung cancer
  • Exogenous hormones
  • Lung disease
  • Drug-SSRI, carbamazepine,
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59
Q

What releases somatostatin and what does it do?

A
  • Hypothalamus since it is AKA Growth Hormone Inhibiting Hormone
  • Inhibits release of GH from anterior pituitary
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60
Q

Prolactin is structurally homologous to:

A

Prolactin is structurally homologous to growth hormone

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61
Q

What inhibits GnRH?

A

Prolactin inhibits the release of GnRH which inhibits ovulation

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62
Q

What inhibits prolactin?

A

Dopamine from the Hypothalamus

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63
Q

Name 6 hormones released from Hypothalamus:

A
  1. TRH
  2. GnRH
  3. GHRH
  4. Somatostatin
  5. CRH
  6. Dopamine
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64
Q

What is somatotropin?

A

Growth hormone

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65
Q

What stimulates release of growth hormone?

A
  • Sleep
  • Hypoglycemia
  • Stress
  • Puberty
  • Exercise
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66
Q

What decreases release of growth hormone other than somatostatin?

A
  • Aging
  • Obesity
  • Hyperglycemia
  • Somatostatin
  • Somatomedin
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67
Q

What is Laron Dwarfism? What causes it?

A
  • Growth hormone receptors are defective
  • No production of Insulin-like growth factors in target tissues
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68
Q

What is the level of GH in Laron Dwarfism? What is the treatment?

A
  • Growth hormone levels are increased in Laron dwarfism, since no IGF are made, negative feedback mechanism
  • Recombinant Insulin-like growth factor-1 is the treatment
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69
Q
  1. Excessive release of growth hormone in adulthood causes:
  2. Excessive release of growth hormone in childhood causes:
A
  1. Acromegaly
  2. Gigantism
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70
Q

What is the treatment for excessive release of growth hormone and why?

A
  • Somatostatin analogues
  • Because somatostatin inhibits the release of growth hormone from AP
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71
Q

Abnormal increased serum IGF-1 indicates:
Why?

A
  • Increased serum Insulin-like growth factors indicates increased release of GH = acromegaly/gigantism
  • IGF-1 is used for diagnosis since GH levels are fluctuating
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72
Q

What can cause abnormal release of growth hormone?

A

Secreting pituitary adenoma

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73
Q

What is Sheehan syndrome?

A
  • Induced form of α-pituitaries
  • Caused by postpartum hemorrhage inducing ischemic infarct of pituitary (mainly anterior pituitary)
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74
Q

A first-time mother is experiencing problems with lactation, amenorrhea, and cold interolance. What could be the cause?

A

Sheehan syndrome since she is post-partum maybe she had posthemorrhagic bleeding
- Since this causes ischemic infarct of pituitary, particular anterior: Lowered TSH, prolactin, LH/FSH

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75
Q

What is pituitary apoplexy?

A
  • Sudden hemorrhage of pituitary gland
  • Often due of pituitary adenoma
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76
Q

The signaling pathway of the following hormones is:
ACTH
LH
FSH
TSH
ADH
MSH

A

Adenylyl cyclase mechanism > cAMP

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77
Q

List 6 endocrine hormones with signaling pathway cAMP?

A
  1. ACTH
  2. LH
  3. FSH
  4. TSH
  5. ADH
  6. MSH
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78
Q

The signaling pathway for the following hormones is:
- GnRH
- TRH
- GHRH

A

IP 3 /Ca+2

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79
Q

List 3 endocrine hormones that follow IP IP 3 /Ca+2 signaling pathway

A
  1. GnRH
  2. TRH
  3. GHRH
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80
Q

What is the signaling pathway for the following hormones:
1. Insulin
2. IGF-1
3. Growth hormone
4. Prolactin

A

Tyrosine Kinase mechanism

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81
Q

List the signaling pathway of the following hormones:

  1. Insulin
  2. IGF-1
  3. Growth hormone
  4. Prolactin
A

Tyrosine Kinase mechanism

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82
Q

What is the endocrine hormones signaling pathway for:
ANP
Nitric Oxide

A

cGMP

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83
Q

What endocrine hormones use cGMP signaling pathway?

A

ANP & NO

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84
Q

Where does most digestion occur?

A
  • Duodenum
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85
Q

Where does most absorption occur?

A

Jejunum

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86
Q

The exocrine activity of the pancreas is:

A
  • Pancreatic juice secretion with digestive enzymes and bicarbonate
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87
Q

What do Acinar cells of the pancreas secrete?

A

Digestive enzymes

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88
Q

Acinar cells of ____________ release digestive enzymes in response to ____________ & ___________.

A
  • Acinar of the pancreas release digestive enzymes in response to CCK & Vagal stimulation from PNS
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89
Q
  • When proteases and phospholipase are secreted from ______________ they are ___________.
  • When amylase and lipases are secreted from ____________ they are ______________
A
  • When proteases and phospholipases are secreted from the acinar pancreas they are inactive
  • When amylases and lipases are secreted from acinar cells of pancreas they are active
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90
Q

Why do persons with CF have difficulty with absorbing Vitamins?

A
  • Particularly fat soluble proteins like A, D, E, & K
  • In CF, the mutated CFTR channels cause pancreatic secretions to become thick and unable to be secreted
  • Therefore they do not reach the small intestine
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91
Q

What is the role of ductal cells in pancreatic secretions?

A
  • Ductal cells arranged along the ducts create an isotonic fluid to the palsma
  • They REABSORB the Cl- that was secreted from CFTR channels
  • Ductal cells secrete Bicarb in exchange for secreting Cl- on the lumenal side
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92
Q

What peptides regulate pancreatic secretion?

A
  • CCK
  • Secretin
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93
Q

Peptides, CCK & Secretin contribute to regulation of pancreatic secretions. What cells stimulates CCK secretion & what happens after?

A
  • I cells secrete CCK in the duodenum
  • CCK induces release of pancreatic enzymes from acinar cells by IP3/Ca+2 stimulation
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94
Q

Peptides, CCK & Secretin contribute to regulation of pancreatic secretions. What cells stimulates secretin & what occurs after?

A
  • S cells in the duodenum cause the release of secretin
  • Secretin acts on ductal cells in the pancreas to release Bicarb and Na+ via cAMP stimulation
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95
Q

What causes release of CCK from ____ cells in the duodenum?

A
  • Protein & fats in chyme stimulate the release of CCK from duodenal I cells
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96
Q

What causes the release of Secretin from _____ cells in the duodenum?

A
  • Highly acidic chyme arriving in the duodenum induces the release of Secretin from S cells
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97
Q

What is the most abundant solute in bile?

A

Bile salts

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98
Q

What are the 2 stages of bile secretion?

A
  1. Hepatocytes secrete primarily bile constituents
  2. Bile ducts add water and bicarb, and Salt
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99
Q

Bile salts are ________________________ meaning they can perform 2 functions essential for fat digestion and absorption:
1.
2.

A
  • Bile salts are amphipathic (have both lipophilic and hydrophobic properties)
    1. Emulsification of fats
    2. Transport of lipids
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100
Q

How do bile salts emulsify lipids?

A
  • Detergent action causes fat granules to break down into microscopic droplets allowing them to be digested effectively
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101
Q

How do bile salts transport lipids?

A

Bile salts carry lipids to intestinal wall in the form of micelles

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102
Q

Bile salts carry lipids to intestinal wall in the form of micelles. List three constiuents of the lipids:

A
  1. Monoglycerides
  2. Fatty acids
  3. Cholesterol
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103
Q

What allows release of bile from the common bile duct?

A
  • CCK stimulates contraction of the gallbladder & relaxation of the Sphincter of Oddi for bile to be created into the duodenum
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104
Q

What is the significance of Enterohepatic circulation?

A
  • Functions for recycling of bile
  • When lipid absorption is complete, the bile salts are recirculated to the liver via this system
    1. Absorption of bile salts from the ileum into portal circulation
    2. Delivery back to the liver
    3. Extraction of bile salts from the portal blood by hepatocytes
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105
Q

Contrast the function of peristalsis vs segmentation contractions

A
  • Peristalsis is for moving chyme forward
  • Segmentation is for mixing of chyme
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106
Q

Describe how NT work in conjunction to control peristalsis

A
  • ACh induces contraction behind the chyme
  • NO relaxes the smooth muscle ahead of the chyme for forward movement
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107
Q

About how long after eating does the migrating motor complex initiate action?

A

~ 3-4 hours after food

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108
Q

What regulates the migrating motor complex?

A
  • Motilin is secreted by the unfed state by endocrine cells of the small-intestine mucosa
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109
Q

What is the gastroenteric reflex?

A
  • The presence of food in the stomach increases the motility of the small intestine
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110
Q

The gastroenteric reflex is when the presence of food in the stomach increases motility of the small intestine. What increases motility and what inhibits it?

A
  • increase: Gastrin, CCK, insulin, motilin, and serotonin
  • decrease: secretin and glucagon inhibit
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111
Q

What is the gastroileal reflex?

A
  • The presence of chyme in the stomach triggers increased motility in the ileum
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112
Q

What two major vitamins are absorbed during the colonic phase of digestion?

A

Vitamin K
Vitamin B12

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113
Q

What initiates defecation?

A
  • Feces filling the rectum initiates local release of VIP & NO to dilate the internal sphincter
  • If not time, the external sphincter will contract
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114
Q

What do enterochromoffin cells release and where are they found?

A

Enterochromoffin cells are all along the GI tract and release serotonin for the release of fluid into the lumen especially the large intestine

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115
Q

What is the orthocolic reflex?

A
  • Causes the urge to defecate upon waking and getting out of bed
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116
Q

What is the gastroileal reflex?

A
  • Chyme in the stomach stimulates ileocecal valve to open and allow remnants in the small intestine to enter the colon
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117
Q

What is the pathophysiology of Hirschpring’s disease?

A
  • There is loss of enteric ganglia beginning at the anus and moving orally
  • Where the enteric ganglia is lost there smooth muscle is contracted and will not relax causing swelling and blockage
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118
Q

What causes osmotic diarrhea?

A
  • If there is malabsorption of solutes, causing water to be pulled into the lumen of the GI
  • i.e. lactose intolerance
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119
Q

Describe exudative diarrhea and its causes

A
  • Diarrhea containing pus or blood
  • Occurs in Inflammatory bowel disease
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120
Q
  1. What commonly causes secretory diarrhea?
  2. Describe the mechanism
A
  • Infection, i.e. commonly Cholera
  • Cholera toxin causes hypersecretion of Cl-
  • This causes water and Na+ to follow
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121
Q

What nerves innervate the internal anal sphincter?

A
  • Parasympathetic: Pelvic N (S2-S4)
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122
Q

What is the site of absorption of ethanol?

A

Stomach

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123
Q

What is the site of absorption of NSAIDs and aspirin?

A

Stomach

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124
Q

Where is Vitamin B12 absorption?
How can malabsorption at this location cause disease?

A
  • vitamin B12 absorbed at the ileum
  • Can be cause of hemolytic anemia
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125
Q

Carbohydrate digestion starts in the mouth. What are other sites of carbohydrate absorption occurring?

A
  • Stomach, up to 40%
  • Small intestine thanks to pancreatic amylase
126
Q

Where is lactose and sucrose digested?

A
  • brush border in the duodenum
127
Q

When lactose is broken down by ______________________, what does it become?

A
  • Lactose is broken down by lactase into glucose and galactose
128
Q

When sucrose is broken down by __________________________, what does it become?

A
  • Sucrose is broken down into glucose and fructose by sucrase
129
Q

Na+/K+ pump moves Na+ into the blood from the epithelial cell in the small intestine. How does Na+ get from the lumen into the cell?

A

Co-transporters
- SGLT 1: Na+ with Glucose or Galatcose

130
Q

GLUT 2 moves glucose, __________, ______________ into the blood from the epithelial cell of the small intestine

A
  • GLUT 2 moves glucose, galactose and fructose from the lumen
131
Q

GLUT 5 moves what in the small intestine?

A

GLUT 5 uses facilitated diffusion for Fructose to move from the intestinal lumen into the cell
After the fructose can further diffuse into the blood

132
Q

What does pepsin do?

A

Acts in the stomach to digest proteins

133
Q

What does enterokinase do? Where does it come from?

A
  • Secreted from brush border, especially in duodenum
  • Activates trypsinogen > trypsin for protein break down
134
Q

What does it mean for trypsin to be “autocatalytic”

A
  • Once trypsin is activated by trypsinogen, the trypsin itself can activate other trypsinogen
135
Q

List 3 processes needed for lipids to be digested

A

Emulsification
Enzymatic digestion
Reconstitution of triglyceride and chylomicron formation

136
Q

Lipase breaks triglycerides into:

A
  • Monoglycerides & Fatty acids
137
Q

Describe micelles

A
  • Disk like complex formed by bile salts to collect and store free fatty acids and cholesterol until they come into contact small intestine epithelial cells
138
Q

Where & what is a chylomicron?

A

Once cholesterols, triglycerides, and proteins are inside the cell they can form chylomicrons that are then absorbed by lacteals for movement through the lymph to the vena cava

139
Q

What does Ferroportin do?

A
  • Involved in iron absorption
  • DMT-1 transporter moves iron from the lumen in to the cell
  • After Ferroportin moves iron out of the cell into the blood stream
140
Q

Describe the mechanism of water and electrolyte absorption

A
  • Driven by the Na+/K+ pump on the basal surface of duodenal cells
  • This creates a gradient for Na+ to be reabsorbed from the lumen side
  • The Na+ co transports Cl- etc. which drives the reabsorption of water
141
Q

Sprue can be categorized as:
1.
2.

A
  1. Nontropical sprue
  2. Tropical sprue
142
Q

What is non-tropical sprue? What is the pathophysiology?

A

Celiac disease wherein there is destruction of microvilli and villi causing decreased absorption

143
Q

What is tropical sprue and what is the pathophysiology?

A
  • Bacteria causing decreased absorption of food even when digested
144
Q

What is the difference between malnutrition in pancreatic insufficiency and sprue?

A
  • Pancreatic insufficiency is problems with digestion
  • Sprue is problem with absorption of even well digested food
145
Q

What is the major difference between reabsorption in the Jejunum and Ileum with regards to electrolytes?

A
  • Jejunum has major reabsoption of HCO3- so that acidosis does not occur
  • Ileium has absorption of NaCl
146
Q

Describe and compare the effect of aldosterone in the colon vs kidney

A
  • In both places Aldosterone induces reabsorption of Na+ & excretion of K+
  • Aldosterone works on the principal cells of the kidney
  • Aldosterone acts on epithelial cells of the colon
147
Q

How is CFTR stimulated for Cl- secretion?

A
  • cFTR is a Gα s protein
  • This means when it is activated > adenyl cyclase > cAMP > PKA
148
Q

What cells secrete intrinsic factor?

A

Parietal cells

149
Q

What do parietal cells secrete?

A

Intrinsic factor and HCl

150
Q

How does E. coli induce diarrhea?

A
  • E. coli toxin generates cAMP & cGMP
  • These induce Cl- secretion from CFTR channels & Na+/water to follow
151
Q

Serotonin is a ______________ and induces secretion by:

A

Serotonin is a secretagogue that induces secretion by IP3/Ca+2 stimulation

152
Q

What are three absorptagogues?

A
  1. Aldosterone
  2. Somatostain & Norepi
  3. Cortisol
153
Q

Aldosterone is an __________________________ that causes absorption. By what mechanism & where?

A
  • Aldosterone is an absorpatgogue
  • Works in the distal colon
  • Cause absorption of Na+ and subsequently water
154
Q

What is another name for the HMP shunt? What is its purpose?

A
  • Pentose Phosphate pathway
  • Purpose is to generate NADPH & an alternate route for oxidation of glucose & ribose 5-phosphate
155
Q

What are the two main stages of Pentose phosphate pathway?

A

Oxidative/Irreversible

Non-oxidative/Reversible

156
Q

What enters the HMP shunt?

A

G-6-P/Glucose-6-phosphate

157
Q

How does PPP contribute in the liver?

A
  • Impt in making cholesterol & FA synthesis in well fed condition
158
Q

What does PPP do in the adrenal cortex?

A
  • Steroid hormone synthesis
159
Q

What is the purpose of PPP related to RBCs?

A
  • Maintains Glutathione in a reduced state
160
Q

List the steps in geration of Ribulose 5 phosphate in HMP shunt

A
  1. Glucose 6 P is transformed into 6 Phosphogluconolactone with enzyme Glucose-6 phosphate dehydrogenase and creates an NADPH in the process
  2. Extra step
  3. 6-Phosphogluconate is transformed into Ribulose-5-phosphate using 6-phosphogluconate dehydrogenase which also generates an NADPH & CO2
161
Q

What pathway is this:

  1. Glucose 6 P is transformed into 6 Phosphogluconolactone with enzyme Glucose-6 phosphate dehydrogenase and creates an NADPH in the process
  2. Extra step
  3. 6-Phosphogluconate is transformed into Ribulose-5-phosphate using 6-phosphogluconate dehydrogenase which also generates an NADPH & CO2
    Which enzyme is most important and why?
A
  • This was the HMP Shunt pathway
  • Glucose-6-phosphate dehydrogenase is the most important enzyme because it is the rate limiting step
162
Q

One of the products of the HMP shunt generates: _____________ ____________ __________ which can be used for building nucelotides

A

HMP shunt generates Ribulose-5-phosphate which can be used in the generation of nucleotides

163
Q

Ribulose-5-phosphate can be used to make Fructose-6 phosphate which can be sent to the Glycolytic pathway. What 2 enzymes are vital for this process? Which half of the PP pathway is this?

A
  • Transketolase
  • Transaldolase
    This is the non-oxidative/reversible reaction stage wherein no NADPH is generated
164
Q

In which stage of PPP is NADPH generated?

A

Oxidative/Irreversible reaction stage

165
Q

High [NADPH]/[NADP+] ratio inhibits what pathway via what enzyme?

A

High [NADPH]/[NADP+] ratio inhibits PPP by allosteric regulation of Glucose-6-phosphate dehydrogenase

166
Q

HMP ______________/______________ stages generate & use Ribose 5-phosphate for what?

A

HMP non-oxidative/reversible reaction stages generate and use Ribose 5-phosphate in rapidly dividing cells like hair follicles, intestinal epithelial cells, & skin cells

167
Q
  1. The _______________/_____________ reaction stage of PPP uses transketolase & transaldolase to rearrange carbons to make:
  2. One of these enzymes requires a coenzyme:
A
  1. The non-oxidative/reversible reaction stages of PPP makes intermediates of glycolysis and Ribose-5-phosphate
  2. transketolase requires TPP Vitamin B1 as a coenzyme
168
Q

How does Glutathione contribute to protection from ROS?

A
  • Glutathione is an antioxidant that converts H2O2 into H20
169
Q

Glutathione provides protection for cells from ROS. What are the steps?

A
  1. H202 undergoes reaction to become water using glutathione peroxidase
    1a. Start with 2 molecules of glutathione, 2 G-SH then is transformed into G-S-S-G b/c it gives away its oxygen
170
Q

List 3 enzymatic antioxidants

A
  • Catalase
  • Peroxisomes
  • Glutathione peroxidase
171
Q

Name 3 non-enzymatic antioxidants

A
  1. Vitamin E
  2. Vitamin C
  3. β carotene
172
Q

Reduced Glutathione protects _______ from ROS. What form does it start out as and what form does it become to transform H2O2 into water?

A
  • Glutathione protects RBCs
    -Starts in its reduced form: 2 G-SH & Becomes oxidized: G-S-S-G
173
Q

For Glutathione to protect RBCs it Starts in its reduced form: ___________ & Becomes oxidized: __________. How is the reduced form regenerated?

A
  • Reduced form: 2 G-SH
  • Oxidized form: G-S-S-G
  • Regenerated by glutathione reductase using NADPH + H+
174
Q

How does the inability to maintain ___________ form of glutathione lead to cell lysis?

A
  • Inability to maintain reduced form of Glutathione leads to increased accumulation of superoxides, predominantly H202, that results in a weak cell membrane and ultimately leads to cell lysis
175
Q

What does Cytochrome P450 have to do with PPP?

A
  • CP 450 uses NADPH generated by the PPP to synthesize and modify steroid hormones, cholesterol, Vitamin D metabolism
  • Also contributes to detoxification of xenobiotics
176
Q

CP 450 uses NADPH generated by the PPP to synthesize and modify steroid hormones, cholesterol, Vitamin D metabolism. What enzyme(s) does it use?

A

Uses Cytochrome P450 Reductase

177
Q

What is respiratory burst responsible for?

A
  • Contributes to phagocytic ability of WBC
  • Uses NADPH from PPP to generate superoxide > H2O2 to breakdown bacteria
178
Q

What causes Chronic Granulomatous disease?

A
  • Lack of NADPH oxidase that removes H+ to make O2 a superoxide
  • Inability to breakdown bacteria.
  • Presenting as persistent, severe, pyogenic infection
179
Q

Chronic Granulomatous disease presents as persistent, severe, pyogenic infection. What causes the pyogenic infection?

A
  • Since the bacteria is not broken down it can proliferate and causes infection & pus build up
180
Q

Synthesis of NO requires what from HMP shunt?

A

NO synthesis requires NADPH that was generated from HMP shunt

181
Q

What is the conformation of double bonds in ______________ fatty acids

A

Double bonds in unsaturated FA is cis

182
Q

What is the interval between double bonds in unsaturated fatty?

A
  • Every 3 carbon interval there is a double bonds
183
Q

Saturated or unsaturated FA, which has a higher melting point and why?

A
  • Saturated FA have higher melting point because they do not have double bonds
  • Unsaturated FA double bonds reduces Tm and contributes to their fluid form at room temperature
184
Q

How to determine if a FA is Omega-6 or Omega-3?

A

Determine which is the omega carbon, however many it is from the terminal carbon

185
Q

Which FA are essential? What does “essential” mean?

A

Omega 6 & Omega 3
Means they must be obtained through the diet

186
Q

What is the central tendon of the diaphragm?

A

Muscle fibers radiate from this tendon to the locations where the diaphragm attaches to the xiphoid, ribs, and lumbar vertebrae

187
Q

Where is the Caval opening of the diaphragm?

188
Q

Where is the esophageal hiatus of the diaphragm?

189
Q

Where is the aortic hiatus of the esophagus?

190
Q

Where do the least and greater splanchnic nerves originate from?

A

Originate from sympathetic trunk

191
Q

The greater and lesser splanchnic nerves pass through the diaphgram:

A

Pass either directly through the muscle or around the L or R crus (posterior attachment of the diaphragm)

192
Q

What is the cisterna chyli?

A

Enlarged vessel in the upper abdominal portion of the “thoracic duct”

193
Q

What is the action of Quadratus Lumborum?

A

Stabilization of the spine

194
Q

Where is a common location of AAA?

A

B/t inferior mesenteric artery and common iliac artery

195
Q

What can cause entrapment of L renal vein?

A

Compression of the L renal vein can be caused by enlargement of the superior mesenteric A. which passes anterior to it

196
Q

Where is referred pain for the kidney?

197
Q

Do the kidneys ascend or desend during development?

A

Ascend from the pelvic cavity and thus share venous supply with testicular & ovary

198
Q

Do ureters descend or ascend through the retroperitoneal region to reach the bladder?

199
Q

The ureters cross anterior or posterior to ________ ____________ A or near their bifurcation into:

A

The ureters cross anterior to the Common iliac arteries or near the bifurcation of common iliac at the external iliac A or internal iliac A

200
Q

The kidney is proximal to what to nerves & what vertebral level do they come out of?

A

Iliohypogastric & ilio-inguinal
Come from L1

201
Q

Where is the cross talk in referred pain?

A

In the spinal cord where the dermatome somatic afferent nerve and the visceral afferent nerve have interacting branches

202
Q

What vertebral levels does the Greater Splanchnic come from?

203
Q

What vertebral level does the lesser splanchnic come from?

204
Q

What vertebral level does least splanchnic come from?

205
Q

Describe the innervation and release of NT from adrenal medulla

A
  • Greater splanchnic innervates the adrenals as preganglionic fibers
  • Since the adrenal medulla secrete Norepi and Epi into bloodstream they are considered post-ganglionic in function
206
Q

What is the endocrine function of adrenal cortex?

A

Adrenal cortex releases glucocorticoids (cortisol) & minteral corticoids (aldosterone)

207
Q

What is proximal blood supply of adrenal glands?

A
  • Superior adrenal from inferior phrenics
  • Middle adrenal from aorta
  • Inferior adrenal from renal A
208
Q

What is the ganglion impar?

A

Where the sympathetic trunk joins at the coccyx and is no longer bilateral along the vertebral bodies

209
Q

What PNS innervates the foregut?

210
Q

What PNS innervates hind gut?

A

Sigmoid & beyond is pelvic PNS (S2-S4)

211
Q

What are the three key ganglion for SNS innervation of the GI?

A
  • Celiac ganglion
  • Superior mesenteric ganglion
  • Inferior mesenteric ganglion
212
Q

What does the Celiac ganglion innervate?

A

Upper GI and adrenal medlla

213
Q

What does the superior mesenteric ganglion innervate?

A

small intestine

214
Q

What is the most distal target of vagus N?

A

Ascending and transverse colon

215
Q

What does pelvic N Innervate?

A
  • Hindgut & pelvic
  • Transverse colon
  • Descending sigmoid colon
  • Rectum, anus
  • Bladder
  • Reproductive tract
216
Q

What does the celiac ganglion innervate?

A

Liver
Gallbladder
Foregut (stomach, duodenum, pancreas)

217
Q

Describe the sympathetic innervation beyond L3

A

Para sympathetic via sympathetic chain with control of blood supply only

218
Q

What does the superior mesenteric ganglion innervate?

A

Midgut including jejunum, ileum, transverse colon

219
Q

What does the inferior mesenteric ganglion innervate?

A

Hind gut & pelvic targets

220
Q

What is the dermatome invovled in referred pain of the gallbladder?

A

T7-T8 on the R

221
Q

What is the vertebral levels is referred pain of the duodenum

222
Q

What is the vertebral levels of referred pain of the appendix?

223
Q

What is the vertebral levels of referred pain of the appendix?

224
Q

What is the dermatome involved in referred pain for kidney, ureter?

225
Q

What is the dermatome level for refereed pain for stomach/pancreas?

226
Q

What are the Islets of Langerhans?

A
  • Collection of cells in the pancreas that secrete endocrine hormones
  • Contain α, β, Δ, and PP cells
227
Q

Which cells of the Islet of Langerhans release glucagon?

228
Q

Which cells of the Islet of Langerhans release insulin?

A

β cells, these cells are in greatest quantity in the pancreas Islet of Langerhans

229
Q

Which cells of the Islet of Langerhans release somatostatin?

A

Δ cells release somatostatin

230
Q

Which cells of the Islet of Langerhans release pancreatic polypeptide?

A

PP cells of the pancreas

231
Q

Insulin is a _______________________ and thus is water soluble.

A

Insulin is a peptide

232
Q

List the 4 steps of cellular action when insulin binds to a cell

A
  1. Insulin binds to the α subunits of the enzyme-linked receptor on a cell
  2. The β subunit of this cell then self phosphorylates
  3. This causes tyrosine kinase to be phosphorylated
  4. Insulin receptor substrates (IRS) begin to phosphorylate enzymes within the cell
233
Q

List 3 major downstream cellular outcomes of insulin binding to cell membrane receptor.

A
  1. Increase fat synthesis in fatty tissue
  2. Protein synthesis
  3. Increase glucose transport into the cell
234
Q

3 Major downstream cellular outcomes of insulin binding to cell membrane receptor are:
1. Increase fat synthesis in fatty tissue
2. Protein synthesis
3. Increase glucose transport into the cell
Describe the significance of upregulating protein synthesis

A
  • In children, this increases growth
  • Since the glucose transporters are peptides themselves, this increases their expression on the cell surface to increase glucose uptake
235
Q

T/F: Insulin increases GLUT1 & GLUT3 uptake of glucose in the brain

A

False, brain glucose levels are not regulated by insulin

236
Q

Which GLUT transporters are insulin independent and where are each respectively?

A
  • GLUT 1: brain & blood-brain barrier
  • GLUT 2: Pancreas, liver, small intestine
  • GLUT 3: Brain, neurons, sperm
237
Q

Which GLUT transporter is involved in diabetic patients? Why?

A
  • GLUT 4 has implications in diabetes because it is a insulin dependent glucose transporter
238
Q

What three hormones increase hormone-sensitive lipase in fats and subsequently increasing the production of fatty acids and glycerol excretion from fat cells

A
  1. Growth hormone
  2. Cortisol
  3. T3
  4. Epinephrine
    all induce the action of lipase to breakdown triglycerides into fatty acids for release as well as glycerol release into the blood
239
Q

In _________________ cells, hormones can induce the action of lipase to breakdown triglycerides into fatty acids for release as well as glycerol release into the blood. What hormone inhibits this?

A
  • In fat cells
  • Insulin inhibits lipase
240
Q

Insulin promotes the production of ________________________________________. What hormone requires insulin presence to work?

A

Insulin promotes the production of protein storage for increasing muscle mass
- Growth hormone increases growth only in the presence of insulin

241
Q

Excessive growth hormone can induce insulin-resistance. List 4 downstream effects of this

A
  1. Increase glucose in blood
  2. Increase FFA in blood
  3. Increase Ketoacids in blood
  4. Increase amino acids in blood
242
Q

Describe the circulating levels of insulin .

A
  • Insulin is only released after eating
  • As plasma glucose levels rise, so does release of insulin
243
Q

Describe how intake of glucose at β pancreatic cells induces release of insulin

A
  1. GLUT2 uptake glucose
  2. Glucose converted into ATP
  3. Increased ATP production blocks ATP/K+ channels
  4. The low lack of K+ leaving allows the cell to depolarize
  5. Depolarization of the cell causes Ca+2 channels to open and increased Ca+2 causes insulin vesicles to dock at membrane and be released from β cell
244
Q

The following factors potentiate the release of insulin:
4. Glucose → ↑ Insulin release
3. Amino acids + Glucose → ↑ insulin release
2. ___________________ + Glucose → ↑ Insulin release
1. ______________________________, ___________________________, ______________________ + Glucose → ↑ insulin release

A
  1. GI hormones
  2. Glucagon, growth hormone, cortisol
245
Q

The following factors have some of the strongest effect in inducing insulin release:
2. GI hormone + Glucose → ↑ Insulin release
1. ______________________________, ___________________________, ______________________ + Glucose → ↑ insulin release
Which GI hormones?

A
  1. Gastrin, CCK, secretin, GLP-1, & GIP
  2. Growth hormone, glucagon, cortisol
246
Q

How do sulfonylureas impact insulin/glucose concentrations?

A
  • Solfonylureas block ATP/K+ channels in β cells of the pancreas
  • This induces the depolarization of the cell & Ca+2 channels open so insulin canbe released from β pancreatic cells
247
Q

Compare and contrasct where insulin acts vs where glucagon acts

A
  • Insulin acts in the liver, muscle, & fat
  • Glucagon only acts in the liver
  • Both are peptide hormones & thus are H20 soluble
248
Q

Where does glucagon bind on the cell to induce glucose release?

A

Glucagon binds to receptors which then binds to a G s receptors to increase cAMP & PKA

249
Q

What are three metabolic effects of glucagon increase?

A
  • Increased plasma glucose levels
  • Decreased amino acid levels
  • Increased ketoacid plasma levels
250
Q

The following factors _____________________ glucagon secretion:
- Amino acids: ________________ & ___________________
- GI hormones: CCK & gastrin
- Exercise
- Neural influences such as:

A

The following factors increase glucagon secretion:
- Amino acids: Arg & Ala
- GI Hormones: CCK & Gastrin
- Exercise
- Neural influences such as β adrenergic stimulation, sympathetic activity, vagal activity-acetylcholine

251
Q

The following factors ____________________ glucagon secretion:
- Somatostatin
- GI Hormones: ________________________, ______________________
- Free fatty acids
- Ketoacids
- Neural influences:

A

The following factors decrease glucagon secretion:
- Somatostatin
- GI hormones: GLP-1, Secretion
- Free fatty acids
- Ketoacids
- Neural influences: α adrenergic stimulation

252
Q

Glucagon and epinephrine can increase glucose release from the liver, how does epinephrine do so?

A
  • Epinephrine simulates sympathetic nerve increase in epinephrine to increase glucose from the liver
253
Q

Describe the mechanism of Type I Diabetes:

A

Caused by loss of β cells, viral infection, or autoimmune = DECREASED Insulin levels

254
Q

List some tissue effects of DM T1

A
  • Urinary glucose
  • Osmotic dehydration
  • Osmotic diuresis
  • Autonomic dysfunction
  • Metabolic acidosis
  • Hypercholesterolemia
255
Q

Aside from increased glucose levels, list 3 additional symptoms of DM T1

A
  1. Increased fat utilization
  2. Protein depletion
  3. Increased thirst
  4. Polyuria
256
Q
  • _______________________ __________________
  • High insulin
  • Obesity
  • Increased triglycerides caused by:
    are all symptoms of:
A
  • increased glucose
  • High insulin
  • Obesity
  • Increased triglycerides caused by increased increased insulin level
    are all symptoms of DM T2
257
Q

Why in type II DM, will there be eventual decrease in insulin level when this is normally considered a disease of insulin resistance?

A
  • If the diabetes is uncontrolled the metabolic effects will destroy the β pancreatic cells and no insulin is released
258
Q

Compare and contrast glucagon levels in DM type I & Type II

A
  • Both have high plasma glucagon levels
  • Type I: High levels of glucagon can be suppressed
  • Type II: high levels of resistance to glucagon are difficult to suppress b/c the α cells that synthesize glucagon cannot be inhibited
259
Q

What is the largest source of calcium?

260
Q

What is the largest source of phosphate?

A

GI absorption

261
Q

What three factors control calcium levels?

A

Vit D
Parathyroid hormone
Calcitonin

262
Q

What do RBCs have to do with Vitamin D?

A
  • Erythropoietin that synthesizes can synthesize Vit D
263
Q

Where is Vit D produced?
Where does it act?

A

Vitamin D is produced in the skin & kidney
Vitamin D acts in the intestine

264
Q

T/F: Vit D is a cholesterol structure and thus is not water soluble

A

True, so the receptors are inside the cell & can diffuse through cell membrane

265
Q

What are the 4 major actions of Vitamin D?

A
  • Promotes intestinal absorption of calcium
  • Promotes intestinal absorption of phosphate
  • Increases renal reabsorption of calcium and phosphate
  • Enhances bone calcification
266
Q

Describe the mechanism by which Vit D induces increased uptake of Ca+2 in the gut

A

Skin makes Vit D 3 → in the liver, Vit D turned to 25-Hydroxycholecalciferol → then in the Proximal tubule of the Kidney, PTH will activate by transforming it to 1, 25 Hydroxycholecalciferol → 1,25- hydroxycholecalciferol will induce intestinal epithelium to increase Ca+2 absorption

267
Q

What is Calbindin?

A

Calcium-binding protein that is necessary for the absorption of Ca+2 in the diet

268
Q

What is the feedback control for Vit D3 regulation of Ca+2 absorption

A
  1. Ca+2 itself can inhibit PTH if levels are too high which stops the production of Active Vit D-1,25-Dihydroxcholecalciferol
  2. Liver can sense if 25-hydroxycholecalciferol is too high and inhibit its production
269
Q

1,25- hydroxycholecalciferol will induce intestinal epithelium to increase Ca+2 absorption, by what cellular mechanism?

A
  • 1,25-dihydroxycholecalciferol has a nuclear receptor in the intestinal epithelium to indcrease protein production for Calbindin for absorption from intestinal lumen
  • Also synthesizes Na+/Ca+2 exchanger on basal cell side
270
Q

Where does parathyroid hormone act?

A

Proximal tubule of Kidney & bone

271
Q

PTH ______________________ phosphate reabsorption & _______________ Ca+2 reabsorption

A

PTH decreases phosphate reabsorption & increases Ca+2 reabsorption

272
Q

PTH is a peptide hormone meaning:

A

Meaning it is water soluble and cannot diffuse through the lipid membrane of a cell

273
Q

What cell types secrete PTH from the parathyroid gland?

A

Chief cells

274
Q

There are _____ parathyroid glands glands atop the thyroid gland. Normal persons can have normal production of PTH with as few as ____ gland.

A

There are 4 parathyroid glands atop the thyroid gland. Normal persons can have normal PTH production with as few as 1 Parathyroid gland

275
Q

How does PTH secretion effect bone?

A
  • PTH levels incresae Ca+2/Phosphate resorption from bone by inducing osteoclast proliferation
  • Excess can weaken bones
276
Q

Describe how PTH impacts Phosphate levels in the body

A
  • PTH increase absorption of phosphate from the bone by inducing osteoclast proliferation
  • Subsequently, it induces increased excretion of phosphate from the kidney
277
Q

What produces calcitonin?
Were does it act?
What is its chemical structure?

A
  • Parafollicular cells of the thyroid
  • Acts on the bones
  • Peptide hormone
278
Q

What is the main action of calcitonin?

A

Opposes effects of PTH
- Overall lowering Ca+2 levels

279
Q

The following are indicative of:
- Decreased osteoclast activity
- Decreased bone calcium resorption
- Decreased plasma calcium
- Low calcium

A
  • Indicative of low PTH, thus hypoparathyroidism
280
Q

Carpopedal spasm can be indicative of hypoparathyroidism, why?

A
  • Low Ca+2 levels
  • Low Ca+2 levels lower the threshold potential making the cell more excitable and increase depolarization. Also cause tetany, seizure, & arrhythmia
281
Q

How can chronic renal disease impact Vit D?

A
  • At the proximal tubule of the kidney is where 25-hydroxycholecalciferol is activated to 1,25-dihydroxycholecalciferol which increases Ca+2 absorption in the intestine
  • If there is damage to renal activity, this can be impaired
282
Q

The following are indicative of:
- Decreased QT interval
- Decreased gastric motility
- Kidney stones
- Increased osteoclast activity

A

Increased PTH → Hyperparathyroidism

283
Q

What is the adult form of Rickets?

A

Osteomalacia due to Vit D deficiency

284
Q

Why are bisphosphonates a treatment for osteoporosis?

A
  • Bisphosphonates kill osteoclasts
285
Q

List three causes of osteoporosis

A
  • Reduce osteoblast activity due to aging
  • Decrease estrogen
  • Cushing syndrome
286
Q

The viscerosomatic reflex for the upper ureter and kidney is at the:

A

The viscerosomatic reflex for the upper ureter and kidney is at the T10-T11 spinal level

287
Q

When a vertebral segment translates to one side, it side bends to the contralateral side. Therefore,

A

Therefore, if the segments freely translate left, it can be deduced they are sidebent right

288
Q

What are dietary sources of sucrose?

A
  • Sucrose Glucose + Fructose
  • From: table sugar, fruit juice, fruits
289
Q

What is a dietary source of fructose?

A
  • Hexose sugar
  • Honey
290
Q

What are 3 metabolic uses of fructose?

A
  • Spermatozoa use for E
  • Can enter glycolytic pathway but do not produce as much energy
  • Fructose can give rise to glucose
291
Q

What transporter is responsible for the uptake of Fructose?
What is the first thing that happens once fructose enters a cell?

A
  • GLUT-5 transports fructose into the cell
  • First thing, fructose is phosphorylated by Hexokinase (muscle) or by Fructokinase
292
Q

Where does fructokinase act?

A
  • Liver, pancreas, kidney, and small intestine
  • Once the fructose is inside the cell, Fructokinase will phosphorylate to Fructose-1-P
293
Q

What type of phosphorylation does Hexokinase do to fructose & where does it act?

A
  • Hexokinase in the muscle will transform Fructose into Fructose-6-P
294
Q

Hexokinase in the muscle will transform Fructose into Fructose-6-P. What is the significance of this?

A

Fructose-6-P can directly enter the glycolytic pathway! For muscle E use

295
Q

Increased dietary fructose promotes increased:

A

Increased dietary fructose promotes increased fatty acid and TAG synthesis in the liver

296
Q

Increased dietary fructose promotes increased fatty acid and TAG synthesis in the liver. Why?

A

Because in the liver, there are no regulated enzymes.
- Since Fructose-1-P can directly enter the glycolytic pathway and bypass the highly regulated PFK-1
- Additionally, the enzyme Aldolase will transform the Fructose-1-P into DHAP & G3P to continue to bypass regulating steps

297
Q

What is the significance of sorbitol dehydrogenase?

A
  • An enzyme in tissue that can convert sorbitol into fructose
  • Sorbitol comes from Glucose that is reduced in the polyol pathway
  • Sorbitol brings in water which damages cells
  • Sorbitol can accumulate rapidly and is reduced slowly to produce fructose
298
Q

What cells lack sorbitol dehydrogenase and thus are at risk for sorbitol accumulation?

A
  • Lens
  • Retina
  • Peripheral nerves
  • Kidneys
    all lack sorbitol dehydrogenase that convert sorbitol to fructose
299
Q

There are two inherited abnormalities in fructose metabolism, name them & their severity.

A
  • Essential fructosuria: benign
  • Hereditary fructose intolerance: significant risk
300
Q

What is deficient in essential fructosuria? Where does the build up take place?

A
  • Lack of fructokinase enzyme to phosphorylate fructose when it enters the cell
  • Fructokinase acts in the liver, kidney, pancreas, and small intestine
  • Can have fructose in the urine, typically harmless
301
Q

What is deficient in Hereditary fructose intolerance? Where does the fructose build up take place?

A
  • Lack of Aldolase B enzyme that transforms Fructose-1-P into DHAP & G3P in the liver, pancreas, kidney, and small intestine
302
Q

What is the mechanism occurring in hereditary fructose intolerance?

A
  • Fructose-1-P is phosphorylated as it enters the cell
  • Trapped in the cell and uses up all the Phosphate in the cell
  • Will induce hypoglycemia during even mild fasting because the body cannot use P for glucagon
303
Q

What is galactose & what is the main dietary source?

A
  • Galactose = Glucose + Galactose
  • Dietary galactose is lactose
  • Galactose must be converted to glucose before it can be metabolized
304
Q

What is the first step in galactose metabolism?

A
  1. Galactose enters the cell
  2. GALK phosphorylates galactose into Galactose-1-P
305
Q

Once Galactose is phosphorylated to Galactose-1-P by Galactokinse (______________), what happens next?

A
  • GALK
    3. Galactose-1-P is converted into Glucose-1-P by GALT
306
Q

In the 3rd step of Galactose metabolism, Galactokinase-1-P is transformed into Glucose-1-P by GALT. Describe the details

A
  • GALT = Galactose-1-P Uridyltransferase
  • GALE brings a UDP-Glucose
  • GALT pulls the glucose off the UDP-glucose and exchanges it for Galactose. It replaces the Galactose for Glucose-1-P
  • Resulting in: Glucose-1-P and UDP-Galactose
  • G-1-P can now enter glycolytic pathway
307
Q

What is the significance of GALE in galactose metabolism and what are some fates of its final product?

A
  • GALE brings UDP-Glucose to exchange the Glucose for Galactose resulting in UDP-Galactose generation
  • UPD-Galactose can be turned back into UPD-Glucose for repeat use
  • UDP-Galactose can be used to synthesize Lactose or GAGs
308
Q

Name the three types of Galactosemia:

A

Each having to do with a deficiency in the enzymes that break down Galactose
- GALK Deficiency (cannot phosphorylate Galactose)
- GALT Deficiency (cannot switch Gal to Glu from incoming UDP-glucose)
- GALE deficiency

309
Q

What is the most severe type of Galactosemia?

A
  • GALT deficiency (cannot make Glucose-1P from Gal-1-P)
  • Most prevalent and most common
310
Q

GALT defciency can be asymptomatic at birth, but cause:
1.
2. ____________________________ & _____________________ with milk consumption
3.
4.
5.
6.

A
  1. Lethargy
  2. Vomiting and diarrhea after milk consumption
  3. Cataracts
  4. Liver damage & Jaundice
  5. Brain damage
  6. Kidney failure

M1 Block 5 (3 decks)

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